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.

Baxter Contact Information

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.

Bergman Contact Information

My lab’s research focuses on the identification of behavioral and physiological processes that involve the neurotransmitter histamine, 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 involving CRISPR mutagenesis of a gene involved in histamine metabolism) 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.

M. Burg Contact Information

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 are 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, phosphor-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, an alterations in the relative quantity of phosphorylated isoforms of GAP-43 might be associated with a pathological biochemical processes.  GAP-43 might serve as a potential new biomarker testing efficacy of drugs designed to treat Alzheimer’s disease.

Capodilupo Contact Information

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.

Cleary Contact Information

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

DeLano-Taylor Contact Information

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.

Fateye Contact Information

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.  I call it intellectual ADHD.  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.

Graham Contact Information

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.

Haley Contact Information

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.

Kegley Contact Information

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.

Kipp Contact Information

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 focused on the impact of fatty acids as some are proinflammatory (saturated and polyunsaturated (trans) fatty acids) while other polyunsaturated fatty acids are anti-inflammatory (omega 3 and cis). We started by evaluating the endothelial cell expression of gap junction protein (connexin 43) responsible for communicating between cells which is upregulated by inflammation.  After 24 hours, saturated fatty acids (palmitic acid) increased Cx43 while omega 3 fatty acids (eicosapaentanoic and docosahexaenoic acids) decreased Cx43 expression.  Blockade of the fatty acid receptor proposed to mediate the anti-inflammatory effects of omega 3 fatty acids had the opposite effect (the inhibitor appeared anti-inflammatory). We are currently evaluating inflammatory signaling molecules to determine whether this unexpected result is reproducible and to attempt to explain the reason for this outcome. 

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.  Although on sabbatical this fall (2021), I would be happy to talk with a student about research questions that they might be interested in addressing in the lab in the future.  I have mentored many student projects (both research and writing) for the honors college.

Kurjiaka Contact Information

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.

Kwesiga Contact Information

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. 

Laudicina Contact Information

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 nicotinic compounds in the treatment of visual diseases, specifically glaucoma.  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 neuroprotection to the cells that are the target of neurodegeneration in glaucoma.  We have also shown that a selective ‘positive allosteric modulator’ (PAM) of the alpha7 nAChR can be of potential benefit.  In addition, we have provided evidence that a compound originally developed to increase ACh release in Alzheimer’s disease was effective in our experiments.  Most recently, we have shown that activation of the alpha7 nAChR can also lead to regeneration of cells lost during the disease process.  We are currently investigating if this regeneration leads to functional recovery of visual function lost during the disease process.  Experiments in my lab have included cell culture, neurotransmitter release studies, and confocal microscopy.  Future experiments could include labeling existing cells to differentiate from ‘regenerated’ cells, applying compounds to rodents as eye-drops, and following functional recovery (via electroretinograms).

Linn Contact Information

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.

Liu Contact Information

Dr. Nochera is interested in developing research with breadfruit not only as an alternative but also as a "functional food" product for the public. Breadfruit is high in starch, rich in antioxidants, and is also gluten free. New breadfruit products can provide nutritious, appealing and inexpensive gluten free food sources based on locally available breadfruit in areas of the world where it can be easily grown.

Nochera Contact Information

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.

Pearl Contact Information

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.

Ramsson Contact Information

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.

Reed Contact Information

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.

Renkema Contact Information 

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.

Plastination Lab Information

Richiert Contact Information

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. 

Shabani Contact Information

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 micro-CT scanning, and processing digital micro-CT 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.

Stroik Contact Information

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 potential sympathomimetics. 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.

Sylvester Contact Information

My research focuses on using Candida albicans as a model fungal pathogen. C. albicans is a frequently acquired nosocomial infection both within the U.S. 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 U.S. 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.

Currently, we are focused on studying a subset of proteins whose level appears to need to change to allow the shape transition that is associated with disease to occur. We are studying this subset on multiple levels including: Which need to change to allow the transition, how this subset influences the ability to cause disease and exactly how the proteins modulate their effect.

Thomas Contact Information

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.

Please see this link for a list of publications.

Thompson Contact Information