BMS Department Faculty Research by Professor
My research focuses on the pathogenic mechanisms of Salmonella and biofilm formation in Escherichia coli. In Salmonella we are currently working toward finding additional genes necessary for Salmonella virulence. Studies have shown that the genes involved in Salmonella pathogenesis are found in specific regions of the chromosome known as pathogenicity islands. Salmonella Pathogenicity Island 1 (SPI-1) has numerous genes involved in the formation of a 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 needed for survival within macrophage after invasion across the intestinal epithelia is completed. Due to the number of genes required for each of these processes to occur, the bacteria tightly regulate their expression. Our lab’s focus is on the regulatory genes that control activation and repression of these islands in response to environmental signals. As part of these studies, I characterized a repressor known as hilE, which represses the activation of SPI-1. Studies of the DNA sequence surrounding hilE suggest that this repressor lies in a 40 kb region of the chromosome that has all the hallmarks of a pathogenicity island, yet little is known about the function of these genes. We created ten different polar mutations in potential operons within this identified region. Work has started trying to analyze the effects these mutations have on Salmonella virulence by using gene reporters, cell invasion, macrophage survival and bacterial adherence assays, etc. all conducted under various virulence inducing and noninducing environmental conditions. Any effects on Salmonella invasion could then be further characterized by identifying how each gene affects Salmonella pathogenesis in response to an environmental signal.
My second project is looking for genes important for Escherichia coli biofilm formation under conditions that mirror the intestinal environment. Earlier 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 a commensal bacteria found in the anaerobic conditions of the colon, we are trying to find regulator genes that may be responsible for increasing or decreasing biofilm formation in response to oxygen concentration. We developed a biofilm assay and are using it to screen a library of nonpolar mutants under aerobic, microaerophilic, and anaerobic conditions to determine if there are effects on biofilm formation at varying oxygen levels.
Dr. Bergman’s research focuses on the intersection of neuroscience, physiology, behavior, ecology, toxicology, histology, and pharmacology. His multidisciplinary lab uses crayfish as a model organism to explore how the nervous system responds to injury, chemical exposure, and environmental stressors. Animal models like crayfish provide powerful insight into human physiology and medicine, forming the foundation for discoveries in neuropharmacology, neural repair, sensory processing, and behavioral neuroscience. Dr. Bergman’s research investigates:
- The effects of drugs, pollutants, and hormones on neural and behavioral health
- Mechanisms of sensory perception and aggression
- How environmental stress impacts neural and hormonal systems
Crayfish offer an ideal balance between simplicity and similarity to vertebrate systems, making them valuable for studying neural plasticity, toxicology, behavior, and physiology. If you’re interested in neuroscience, physiology or environmental health, and don’t mind a few claws, Dr. Bergman’s lab offers an engaging opportunity for discovery.
I am first and foremost an integrative organismal biologist, with a primary interest in the deep understanding of animal communication systems. I believe that the best research approach is multiscale, from the physics of sensory organs, to how species fit into broader ecological and evolutionary patterns. My scholarship is situated in many fields, including physiology, biophysics, behavior, ecology, and evolution. With this background, I leverage a variety of methods to elucidate the proximate how of a phenomenon within the important evolutionary context of the why.
My lab works primarily in arthropod communication systems, with past projects including the biophysics of cricket hearing, the physics and ecology of cricket sound production, and understanding how temperature influences the physiology and mating behavior of jumping spiders. My lab currently focuses on the jumping spider locomotion system. This unique “semi-hydraulic” system is used both in locomotion (especially jumping) and in flashy sexual display “dances”. My lab seeks to understand how both natural and sexual selection interact to influence this unusual locomotion system. I approach this system from a variety of angles, including: (1) behavioral experiments evaluating courtship and mating behavior, (2) morphology studies measuring different aspects of the external morphology and internal locomotion system, and (3) high speed camera studies of jumping and other types of movement. There are many potential approaches to study this topic, and many projects for undergraduates in my lab. I am eager to speak with students and brainstorm potential project ideas.
My lab’s research focuses on the identification of behavioral and physiological processes that involve the neurotransmitter histamine or its metabolites, using the fruit fly Drosophila melanogaster as a model system . The gene required for histamine synthesis encodes the enzyme, Histidine decarboxylase ( Hdc ). We are currently examining the role of the Hdc gene in establishing when and where histamine is synthesized in a number of cell types, from cells in the central brain to those in the accessory gland (male prostate gland). We continue to examine what the function of histamine (and its metabolites) may be regarding central brain function and its consequences on behavior and reproduction. As a result, projects in my lab range from molecular biology projects (currently characterizing a CRISPR-induced m-Cherry tagged version of the AANATL-7 gene) to microscopy-based and behavioral-based projects. Students interested in becoming part of our research group should contact me, as students are accepted anytime of the year.
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, monkey, and rabbit. We are interested to see if any differences in the profile of GAP-43 are associated with Alzheimer’s disease, a human neurodegenerative disorder characterized by profound cognitive impairment. Since human brain tissue is difficult to obtain, we are utilizing primate brain tissue to establish best practice of visualizing GAP-43 isoforms by two dimensional SDS polyacrylamide gel electrophoresis with the goal of eventually testing the hypothesis that the profile of phosphorylated isoforms of GAP-43 is changed in the brains of a human brain affected by severe cognitive impairment (such as Alzheimer’s disease). Isoforms of monkey brain GAP-43 will be detected by immunocytochemistry, phospho-specific staining, and, further, quantified by computerized densitometry. We believe the phosphorylated isoform of GAP-43 may serve as an indicator of synaptic efficacy and, compared to normal, alterations in the relative quantity of phosphorylated isoforms of GAP-43 might be associated with pathological biochemical processes. GAP-43 might serve as a potential new biomarker testing efficacy of drugs designed to treat Alzheimer’s disease.
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.
Where I came from: Before joining GVSU in 2008, I worked with Sean Morrison and the Howard Hughes Medical Institute to demonstrate that the protein called “Notch" was necessary for directing differentiation of stem cells of the nervous system into glia during development. This work allowed me to integrate my expertise in protein chemistry during my PhD work (protein kinases and phosphoproteins) with cell signaling and neural cell biology.
Why GVSU is special: My lab’s research efforts have been shaped by the mission of my institution and what we love: training the next generation of scientists through excellent pedagogy in the classroom and pursuing pressing questions at the bench. My lab is staffed by undergraduate and masters level researchers (35% first generation college students; 85% of my students went on to attend graduate or professional school, all are employed in the biomedical field). Training affects the scope and speed of our progress, but the supportive environment here allows us to ask high-risk questions with an extended timeline. Further, we can leverage our discoveries to larger collaborative projects to solve important questions in biology (students love being a part of this scientific teamwork).
What we do: My lab works to determine how neural stem cells differentiate into specific cell types during development.
Recently we applied in ovo electroporation to identify that the bHLH gene Nato3 can promote dopamine (DA) neuron related genes in vivo, and that phosphorylation-mimicking modifications of this gene (dubbed “PM-Nato3”) can broaden the efficacy of Nato3 to drive these genes broadly in the CNS. The dopamine neuron relate genes that are upregulated include those that are important in DA neurogenesis and protection of DA neurons from conditions that mimic Parkinson’s disease.
Thus PM-Nato3 has the potential to make DA neurons for PD patients and/or protect PD patient’s DA neurons from further degeneration.
This work has led to a patent filing, support from the NIH, NSF, as well as the Michigan Economic Development Corporation to identify therapeutic and commercialization potential.
We currently have three main interests:
- The mechanism of Nato3 action on promoting expression of DA neuron related genes (Campbell Foundation supported work within our lab).
- Using PM-Nato3 to differentiate human embryonic stem cells into DA neurons (MEDC supported collaboration with University of Michigan’s human stem cell and genome editing core facility).
- Using PM-Nato3 to protect dopamine neurons from parkinsonian conditions in cell culture and in animal models (NIH supported collaboration with Patrik Brundin at Van Andel Research Institute and Jeffery Kordower at Rush University).
My expertise in developmental cell biology and protein chemistry are best illustrated in the following publications and patent filings:
von Linstow CU, Delano-Taylor MK, Kordower JH, Brundin P., Does Developmental Variability in the Number of Midbrain Dopamine Neurons Affect Individual Risk for Sporadic Parkinson’s Disease?Jan. 2020 : 405 – 411.
Peterson DJ, Marckini DN, Straight JL, King EM, Johnson W, Sarah SS, Chowdhary PK, DeLano-Taylor MK., The Basic Helix-Loop-Helix Gene Nato3 Drives Expression of Dopaminergic Neuron Transcription Factors in Neural Progenitors Neuroscience 2019 Nov; 421:176-191
Taylor MK, Yeager K, Morrison SJ., Physiological Notch signaling promotes gliogenesis in the developing peripheral and central nervous systems. Development 2007 Jul; 134(13):2435-47
Taylor MK, Straight J, Peterson D, Huisingh N, Doyle D., Nato3 mutant polypeptides and uses thereof. International Patent Application No. PCT/US16/62876 Unpublished (filing date Nov. 20, 2015).
Taylor MK, Uhler MD., The amino-terminal cyclic nucleotide binding site of the type II cGMP-dependent protein kinase is essential for full cyclic nucleotide dependent activation. Journal of Biological Chemistry 2000 Sep 8;275(36):28053-62
The Fateye lab research focuses on environmental toxicology with the aim of developing context-specific indicators of environmental impact. His lab utilizes a multidisciplinary approach (analytical, genomics and bioassays) to study the toxicity and/or ecological impact of environmental pollutants in vertebrate and invertebrate models. On-going projects in his lab focus on (i) the impact of antibiotics on aquatic microbial ecology and clinical drug resistance in agricultural areas in Michigan; (ii) impact of microplastic pollutants from Lake Michigan on the toxicity to the roundworm Caenorrhabditis elegans. His previous research areas include clinical and epidemiological studies of drug-resistant Plasmodium falciparum malaria, and in vitro/ in vivo studies of photodynamic therapy in models of prostate cancer. Dr. Fateye teaches Pharmacology, Physiology, and introduction to biomedical science research.
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, recruit students to help answer it, then after a year or two move on to something (often completely) 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, microevolution of rabies virus in Michigan bat populations, the population dynamics of raccoon roundworm in West Michigan, modeling Ebola diffusion in West Africa, and social evolution in bacteria. Currently, my lab is using the nematode C. elegans to investigate how the gut microbiome modulates the severity of viral infection.
During the infectious process, a battle ensues between the human host and the bacterial pathogen over access to 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 influences disease outcomes. The primary pathogen I study is 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 biofilm formation, metal acquisition, and metal detoxification in S. lugdunensis.
My research focuses on the effects of sex and gender on long-term trends in human health and mortality. Illuminating the biological mechanisms underpinning sex-specific disease patterns across time is vital for interpreting the drivers of past and present sex- and gender-related health disparities. Therefore, my research program includes projects on both historical and contemporary human populations. I have several ongoing projects that are well-suited to provide research experiences to students interested in human microbiomes, sex-specific patterns of oral and systemic disease, and skeletal maturation and growth.
I am currently investigating how hormonal fluctuations in females impact their oral microbiome and downstream health. My aim is to identify how individualized hormonal shifts affect changes in microbial signatures overtime using saliva and urine samples taken over the course of a menstrual cycle. This project will help identify the factors influencing oral microbial dynamics and the mechanisms behind oral disease manifestation.
I am also working to understand how sex-specific patterns of skeletal growth and maturation are affected by environmental and cultural pressures by using computed tomography (CT) scans from a documented postmortem population. This project is working to identify the effects of early life stressors on skeletal maturation and the timing of pubertal events. This project strengthens our knowledge of the interrelationships between skeletal and dental development and soft tissue indicators of human maturation. This is critical to the documentation of variation in patterns of sexual maturation and growth in past human populations.
Lastly, I am identifying long-term drivers of sex-specific trends in health and mortality using the ancient human oral microbiome, skeletal indicators of disease, and demographic analyses. This project uses ancient DNA sequenced dental calculus taken from medieval and post-medieval Londoners.I use hazards-based statistical modeling to understand how variation in oral microbial diversity across demographic groups in London influenced differential mortality and survival in this context. This project advances our understanding how human-microbial interactions influenced health outcomes in the past.
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.
Fascial release is a popular technique in the strength and performance community. Several methods are reported to increase strength, mobility, and recovery (Body Tempering, roam rolling, Graston©, Reflex Performance Reset, Rolfing). My current interests are in looking at these techniques and assessing their efficacy.
The initial investigations will focus on Body Tempering. In Body Tempering, static or shear heavy compressive forces (20-220 lbs.) are applied to tissues to stimulate changes that will stimulate adaptations that render it more resilient to heavier loads. It is proposed that tempering initiates tissue remodeling according to Wolff’s Law, Davis Law, and the Specific Adaptations to Imposed Demands (S.A.I.D Principle). Wolff’s Law states that mechanical stimulus stimulates bone remodeling (strengthening) and Davis’s Law states that soft tissue will adapt and heal in response to a given mechanical stress. The S.A.I.D. principle is applied to explain that all tissue will respond to mechanical stress by increasing strength and resistance. Tissue tempering is initially applied stimulate tissue to adapt to heavier loads in order to prevent injury. Secondarily it is used to reduce tissue tightness and improve blood flow through local reactive hyperemia. With these purported benefits of tempering, there is a lack of scientific data to back up the claims.
Initial investigations of the range of motion around joints will be used to assess tissue tightness, as well as the measurement through specific exercise movements. This will be accomplished using goniometers and a linear displacement accelerometer (OpenBarbell V3). The effects of tempering on muscular strength will be assessed using a Biodex Balance System SD.
My aim is to understand and learn the methodology of tissue tempering in order to measure its effectiveness for increased mobility and muscular strength. Future research into the other named procedures will be done and we will compare and contrast their efficacy and work to explain any results we may obtain.
My research is generally focused on studying of the impact of inflammatory responses on blood vessel function. This involves directing undergraduate and graduate student research evaluating the response of cultured blood vessel cells (endothelial or smooth muscle) to compounds purported to stimulate or inhibit inflammation. Recently, we have focused on the impact of angiotensin II and angiotensin 1-7 on endothelial cell proliferation/apoptosis. The reason for this focus is that we know angiotensin II decrease capillary and arteriole density (number of these vessels) in the tissues (brain and skeletal muscle) of people with hypertension (the elevation of blood pressure in many individuals is caused by angiotensin II). Interestingly, one of the alternative fates for angiotensin I (angiotensin 1-7) has the opposite effect as it works through a different receptor (mas) than angiotensin II (AT-1). While the impact of angiotensin II on capillaries is clear (reduced number), the mechanism by which they cause this reduction in capillary density are unclear. As this involves a change in the number of endothelial cells, it must involve some combination of a decrease in endothelial cell proliferation or an increase in apoptosis (cell death).
In addition to the specific question above, my broad training in exercise and comparative physiology has provided me with the background to address many other questions. If you are from the honors college, consider either collecting data in my lab or writing a research paper focused on your area of interest (your question), which may be far afield from the cardiovascular system.
My research focuses on assessing cell response to novel therapeutics in physiological and pathological invitro cell culture systems with an emphasis on cardiovascular applications.
Students working with me will have a better understanding of the body’s response to treatments using clinically relevant research models and develop transferable skills that will promote excellence in their career interests.
My research focuses on how bony morphology can inform us about behavior. Using 3D animation modeling, I reconstruct birth mechanisms in human, fossil, and extant primate species in order to better understand how and why human childbirth can be difficult. Students working with me can learn these virtual reconstruction processes while working on pelvic morphology projects.
My research at GVSU has largely been an extension of my previous work at Pharmacia/Upjohn/Pfizer. We have been exploring the possible therapeutic benefits of nicotine-like compounds in the treatment of visual diseases, specifically glaucoma. Acetylcholine (ACh) can activate several subtypes of nicotinic ACh receptors (nAChR) and we have been interested in the alpha7 subtype. Our previous studies have shown that selective activation of the alpha7 nAChR can provide protection to the cells that are normally the targets of death during glaucoma. Most recently, we have shown that activation of the alpha7 nAChR on other cells can lead to the generation of new cells that could replace those lost to disease. We have been examining this mechanism with a multi-step cell culture approach. After obtaining pig eyes from a local slaughterhouse we culture retinal pigment epithelium (RPE, cell layer behind the retina). Then, after stimulating (or not) the RPE with the compound we transfer RPE to a different culture dish of cells from the pig retina. Finally, after a defined time, we count if the stimulated RPE can induce more cells vs. non-simulated RPE. We are currently staining with selective markers (e.g. Ki67 for proliferation) to characteristic the generation of new retinal cells.
Cells detect and respond to external signals (such as an increase in temperature or nutrients) by activating certain intracellular proteins. When the environmental cues are gone, these proteins must be inactivated to avoid overreaction of the cells. Inactivation of proteins is in part through their degradation. Research in my laboratory focuses on the function of one protein named dual-specificity phosphatase 8(DUSP8) in the heart. My prior research has demonstrated that if DUSP8 level is abnormally high in the experimental mice, it will lead to heart failure. This data suggests that DUSP8 protein level must be tightly controlled. Preliminary study performed here at GVSU showed that half of the total DUSP8 proteins was lost after 6 hours (Fig. 1). One explanation for the loss of DUSP8 protein is its degradation over time. The overall goal of this study is to investigate the cellular mechanism controlling the degradation of DUSP8. Specifically, this study will determine whether PEST amino acids within DUSP8 protein serve as the destruction signal to recruit other proteins for DUSP8 degradation.
My research is in paleoanthropology where I investigate questions about human evolution. I am specifically interested in the evolution of upright walking, or bipedalism. I study how bipedalism evolved by combining modern human and primate biomechanics of the knee joint with 3D shape analysis of the bones to interpret the fossil record.
I am also actively involved in field research at the site of Kromdraai Cave in The Cradle of Humankind in South Africa. This site preserves fossil hominin remains from approximately 2 million years ago.
The overall focus of my research is to investigate the role of hormone 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 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 receptors 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. 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. Projects in my lab investigate the effects of estrogen signaling throughout the lifespan (i.e. development, adulthood, aging) using rodent models.
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) characterize the effects of various substances on dopamine neurotransmission in the mouse brain, such as melatonin and CBD.
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 research investigates the microbial impact on immune development and function. When immune machinery functions properly, it is a potent weapon. When the machinery fails, the host is at risk for developing immune disorders like allergies and cancer. The prevalence of these immune disorders has drastically increased over the past few decades, particularly in areas with high sanitation standards and therefore decreased exposure to various microbes like viruses, bacteria, fungi, and parasites. Many researchers have developed hypotheses to explain this. One popular hypothesis is the hygiene hypothesis—basically, that the increase in cleanliness can have unintended, harmful consequences to the immune system.
My lab investigates the hypothesis that microbial exposure impacts innate and adaptive immune cell numbers, activation, and function in the context of cancer. We compare the immune systems of mice with little/no microbial experience and mice with extensive microbial experience. Our lab has shown that mice with increased microbial experience have corresponding increased innate and adaptive immune activation. We recently expanded these findings to a mouse model of melanoma. Microbially experienced mice have slower tumor growth, increase time of survival, and increased tumor-infiltrating immune cells. My lab continues to use this model to investigate the immune mechanism(s) resulting in increased anti-tumor immunity.
I am the current director of the GVSU Plastination Lab. We produce plastinated anatomical specimens (both human and animal) for use in Biomedical Sciences and Biology laboratory courses. Each specimen needs to be meticulously dissected before the process of plastination begins. Most of these dissections are performed by GVSU students. After the specimens have been plastinated, they require positioning to best demonstrate their various structures. Finally, the ‘plastic’ in the specimens needs to be hardened. When all is complete, we have created a marvelous teaching resource that, with gentle handling, can be used for many years.
My broad research interests are on genetic risks of drug use disorders and the associated neural substrates that influence specific aspects of drug use such as, drug taking, seeking and relapse. Methamphetamine (MA) use like that of opioids is a widespread problem in U.S. and is highly addictive drug with devastating consequences for the individual and society at large. My research program explores binge MA use, MA withdrawal and relapse using a genetic mouse model for high and low MA intake. The main aim of my research is to identify and explore druggable targets for future development of therapeutic interventions. Extensive work by my collaborator at Oregon Health & Science University, and her group, who developed this mouse model system have identified at least two quantitative trait loci (QTL) associated with MA intake, located in chromosome 10 and X. In particular, two gene candidates located in the chromosome 10 QTL, namely a u-opioid receptor and a g-protein coupled receptor, known as trace-amine associated receptor TAAR1, seem to play an important role in the MA intake, and other correlated traits. Correlated behavioral traits of interest involve: sensitivity to rewarding and aversive effects through procedures such as, conditioned place preference, conditioned place aversion, conditioned taste aversion; drug reinforcement such as the operant self-administration paradigms; drug withdrawal in form of anxiety and depression-like symptoms tests, such as, zero or plus-maze, forced-swim, and tail-suspension. Recent pharmacological manipulations of TAAR1 receptor in a number of these experiments seem to support the hypothesis that TAAR1 receptor plays an important protective role in MA use and therefore is a prime druggable target to explore in the future. In sum my lab pursues neuroscience related questions mostly at the behavioral genetics, physiological, neurochemical, and pharmacological level.
My primary research interest lies in understanding the ecological mechanisms that drove changes in community composition and structure throughout mammalian 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 are currently exploring two different aspects of mammalian evolution: (1) dietary reconstruction through the study of dental anatomy and (2) microfossil collection and curation. (1) Students interested in dietary reconstruction will prepare dental molds for casting, cast dental specimens from these molds, curate molds and casts, mount dental casts for micro-CT scanning, process digital micro-CT scans, and collect two- and three-dimensional data using imaging software. (2) Students interested in microfossil collection will process sediment from the Uinta Basin, Utah and identify fossils in that sediment using microscopy. These fossil finds fill in an important gap in the vertebrate fossil record during a period of significant global warming ~40 million years ago. Finally, students working in my lab also have the opportunity to conduct paleontological fieldwork in the Uinta Basin, Utah.
Currently, my research focuses on the effects of dietary supplements on the circulatory system. I am most interested in determining the changes in blood flow regulation within the vasculature upon acute exposure to physiological levels of potentially vasoactive nutrients. 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 nutritional supplements in cardiovascular health.
My research investigates how primates integrate behavioral and physiological adaptations to overcome ecological challenges in their natural environment. I aim to integrate how these different facets of animals’ biology work together at the organismal level.
Within this framework, my research program focuses on understanding how wild animals thermoregulate, including how thermal pressures from climate change impact this process. My research in this area has covered behavioral mechanisms such as microhabitat choice and use of postures, hormonal mechanisms of thermoregulation, and non-invasive assessment of body temperature via infrared thermography.
My research also investigates the sensory ecology of foraging decisions. I am interested in how primates use olfactory signals to select foods and communicate information about resources. This research has covered exudate feeding by common marmoset monkeys and seeding eating in pithecids.
My lab provides opportunities for students to gain experience in hormone analysis, behavioral observation methods, thermoregulatory research, and international fieldwork.