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  Mentored Summer Program Research Areas  

Mentors at UAMS

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Mechanisms of Chemotherapy-Induced Cognitive Impairment
Antiño R. Allen, PhD
Division of Radiation Health, University of Arkansas for Medical Sciences

Chemotherapy is commonly used in the management of cancer, but its effectiveness is limited by the potential for injury to normal tissues. Chemotherapy induced cognitive impairment, also Referred to as“chemobrain”or“chemofog,”is experienced by 15 – 80% of cancer patients and survivors.  The Allen laboratory is interested in understanding the mechanisms that are responsible for behavioral toxicities after cancer therapy.  We currently have two active projects; the first is studying how chemotherapy after breast cancer affects cognition in adult female mice.  The second project is investigating the neurocognitive late effects after acute lymphoblastic leukemia chemotherapy in a juvenile mouse model.  Trainees in my lab learn and use a variety of techniques including: behavioral studies, molecular biology (PCR), biochemistry (protein expression, Western blots), immunohistochemistry, histology, light/fluorescent microscopy, cell culture and electrophysiology (brain slice recording) in order to answer questions at multiple levels of the investigation.
Bioinformatics students - No



Glycosylation Changes in Human Cancers
Karen L. Abbott, PhD

Department of Biochemistry, University of Arkansas for Medical Sciences

The Abbott lab studies glycosylation changes on glycoproteins that occur in human cancers. Current areas of study in the lab are (i) identification of glycoproteins and glycan structures that are potential biomarkers from human cancer tissues and plasma using mass spectrometry methods, (ii) development of biomarker detection assays capable of detecting the protein and glycan components of glycoprotein biomarkers for the early detection of cancer in patient plasma, (iii) in vitro and in vivo studies to explore the functional roles of tumor-specific glycosylation changes in the development and progression of breast and ovarian cancer.
Prerequisite courses: Chemistry or Biochemistry
Bioinformatics students: Yes


Alzheimer Disease: Connections to Diabetes and Obesity

Steven W. Barger, PhD
Departments of Geriatrics, Neurobiology & Developmental Sciences, and Internal Medicine
University of Arkansas for Medical Sciences

The Barger laboratory studies basic elements of cellular neurobiology, particularly as they relate to the development of Alzheimer's disease. Using cell cultures and transgenic mice, Dr. Barger and coworkers examine the ways in which the Alzheimer amyloid protein perturbs blood glucose levels and other elements of metabolism outside the brain.  It is hypothesized that these “peripheral” perturbations, in turn, impair brain function in Alzheimer’s disease.  An aspect of the project involves testing new drugs that might alleviate these abnormalities.

Pre-requisite courses:  No

Bioinformatics students:  Yes


DNases in Tissue Injury
Alexei G. Basnakian, MD, PhD
Departments of Pharmacology and Toxicology, University of Arkansas for Medical Science

Cell death is commonly associated with the enzymatic fragmentation of DNA. This includes a limited number of premortem DNA breaks (leading to cell death) and a huge number of postmortem DNA breaks (resulting from cell death). Cells have excessive DNA-degrading power provided by the recently recognized group of cell death DNases/endonucleases which includes: deoxyribonuclease I, deoxyribonuclease II, caspase-activated DNase, endonuclease G, DNase gamma and a few other enzymes. Sometimes these enzymes are called “apoptotic endonucleases,” however they participate in necrosis, mitotic catastrophe, anoikis, and disregulated autophagy as well. Other roles of the DNases include clean-up after cell death, removal of foreign DNA inside the cell, and cleavage of DNA circulating in plasma and other body fluids. Normally, host DNA is protected against these DNases. However, during cell injury or disease, genomic DNA becomes accessible to cell death DNases. Our group tries to identify endonucleases which participate in premortem DNA fragmentation in kidney tubular epithelium during ischemic or toxic acute renal failure, and breast cancer or prostate cancer cells during drug-induced apoptosis. Our studies strongly indicate that the inhibition or inactivation of some of the DNases are protective against cell death in different models. We have recently discovered several specific chemical inhibitors of endonucleases and test if they can be applied as drugs to protect healthy tissues against various types of tissue injury.
Pre-requisite courses: None
Bioinformatics students: Yes


Understanding Lung Cancer Metabolism
Gunnar Boysen, PhD

Department of Occupational Health and Safety, University of Arkansas for Medical Sciences

The Boysen lab interested in understanding the interplay between chemical exposure and nutritional or lifestyle habits, such as diet selection and physical activity. To achieve this we utilize DNA and protein adducts to study carcinogen metabolism, how it is modified by nutritional components and the underlying mechanisms regulating corresponding enzyme activities. In addition studies investigate exposures related changes in common metabolic pathways, using targeted and un- targeted mass spectrometry based metabolomic approaches. The long term goal is to improve our understanding of lung carcinogens and to improve lung cancer therapy.
Bioinformatics students:  Yes


Using Molecular Genetics to Study Virulence in Pathogenic Borrelia
Jon Blevins, PhD

Department of Microbiology & Immunology, University of Arkansas for Medical Sciences

Pathogens of the genus Borrelia are spirochetal bacteria transmitted to humans via the bite of an infected arthropod.  There are two diseases, Lyme disease and relapsing fever, which are commonly associated with Borrelia infection in humans.  Despite intensive research efforts studying the Borrelia that cause Lyme disease and relapsing fever, there is still significant progress to be made towards understanding pathogenic mechanisms that these bacteria utilize to cause disease, colonize tick vectors, and transmit during tick feeding.  Specifically, we are working to determine how Borrelia controls the expression of its genes as it moves between tick and mammal and define contributions of individual Borrelia genes to bacterial virulence and tick colonization.  One of the most direct approaches to demonstrate a causal relationship between a bacterial gene, its cognate gene product, and a requirement during the bacterial lifecycle is to create Borrelia strains in which specific genes of interest have been inactivated.  The abilities of these mutant strains to colonize animals and ticks can then be assessed experimentally to determine whether a given mutant is no longer competent for infection.  Once bacterial factors required for Borrelia infection or tick transmission have been identified, we can begin to study their physiological contributions to these bacterial processes.  In addition, since these factors are known to be essential during the bacterial lifecycle, they also represent viable targets against which therapies could be developed to prevent or treat disease. 
Pre-requisite courses:  Microbiology (Preferred)
Bioinformatics students:  No


Biomedical Semantics: Making Research Data More Flexible

Mathias Brochhausen, PhD, MA

Division of Biomedical Informatics, University of Arkansas for Medical Sciences

My research group works on using Semantic Web Technologies to further medical data managements and research data extraction. This creates data resources that are more flexible than relational databases and allows using automatic inference to integrate data. One key element of this research is to use representational models of the specific domains that are build using best practice approaches. These models are called ontologies. Building ontologies for biomedicine requires the ability to analyze biological and medical sources of information (textbooks, publications, databases, etc.) and extract the subjects of that knowledge. The knowledge gained from this effort will be formalized using the Web Ontology Language (OWL). We will provide the necessary training and training material to enable students to work with Web Ontology Language (OWL). 
Pre-requisite courses:  None (some grasp of formal logic is an asset)
Bioinformatics students:  Yes


Dynamics of Regulation and Function of Diverse Subsets of Anterior Pituitary Cells
Gwen V. Childs, PhD

Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences

Classical studies of the anterior pituitary have shown 6 major cell types with unique neuropeptide releasing hormones as regulators from the brain. However, sensitive molecular assays show that pituitary cells are much more diverse than previously believed. Currently the funded projects in Childs laboratory focus on two examples of this diversity. The first study focuses on the significance and regulation of leptin by specific pituitary cells. Leptin is an appetite regulatory peptide normally produced by adipose cells. However, it might also be a cytokine in the pituitary, working locally to regulate pituitary cells. One project even looks at the possibility that it might be an endocrine factor, produced by gonadotropes to help regulate the reproductive system. The second study focuses on how pituitary cells integrate responses so that a cocktail of hormones is released to meet the needs of a particular physiologic state. Co-expression of multiple neuropeptide receptors is one of the ways the cells can meet these needs and this is regulated by gonadal steroids. The studies use molecular cytochemistry and cytophysiology with a focus on the analysis of individual cells.

Pre-requisite courses:  Cell Biology

Bioinformatics students:  No

9UAMS Molecular Mechanisms of DNA Damage Tolerance in Cancer
Robert L. Eoff, PhD
Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences

The Eoff laboratory explores mechanisms that allow tolerance of DNA damage that would otherwise block normal cellular processes. We use a variety of approaches to investigate the structure and function of translesion DNA polymerases, enzymes that facilitate bypass of DNA damage and other endogenous barriers to replication (e.g. G-quadruplex DNA). Studying the relationship between aberrant activation of DNA damage tolerance and adverse outcomes for cancer patients (e.g. progression to malignancy, resistance to therapy, and maintenance of the cancer stem cell niche) is a central theme in the laboratory. Our work is supported by the National Institutes of Health, and we have an ongoing collaboration with the laboratory of Prof. Peter Crooks (UAMS, Pharmaceutical Sciences) to develop small-molecule inhibitors of translesion DNA polymerases in an effort to potentiate existing drugs used to treat a variety of cancers. We also collaborate with Prof. Kevin Raney (UAMS, Biochemistry) to investigate the proteins and enzymes that participate in G4 DNA maintenance. Through our research, we hope to contribute new insights into mechanisms that are central to mutagenesis, cancer biology, antibiotic resistance, and evolution.
Pre-requisite courses: None
Bioinformatics students:


Mouse Models of Cancer
Aime T. Franco, Ph.D.
Department of Physiology and Biophysics, University of Arkansas for Medical Sciences

In the Franco laboratory we are investigating the role of oncogenes, hormones and microbes in the development of cancer.  We use a variety of mouse models complemented with in vitro cell models to better understand initiation, progression and metastasis of cancer.  We are particularly interested in investigating how different genetic mutations can lead to the development of different subtypes of thyroid cancer.  Although the observed mutations occur in the same cell types, and activate the same pathway, the resultant disease is very different.  We have recently shown that Ras versus Braf mutations lead to the development of different tumor microenvironments and recruit different immune cells into thyroid tumors.  We hypothesize that the immune cells act to suppress the immune response, and promote tumor progression and metastasis.
Pre-requisite courses: None
Bioinformatics students: Yes


Virus-Host Interactions in Gammaherpesvirus Infections
J. Craig Forrest, PhD
Department of Mircobiology & Immunology, University of Arkansas for Medical Sciences

Virology, cancer biology, immunology! Gammaherpesviruses, such as Epstein-Barr virus and Kaposi sarcoma-associated herpesvirus, are cancer-causing viruses that infect the majority of humans. We are working to define functions of viral proteins in infection and disease, identify host factors that block viral infection and prevent virus-driven cancers, and understand immune responses to chronic viral infections. We use a multi-disciplinary approach that includes basic cell biology, molecular genetics, global proteomics, and mouse models of infection to accomplish our major goal of defining the complex relationship between gammaherpesviruses and their hosts. PLUS, we get to do cool science and figure out how stuff works!
Pre-requisite courses: Biology and Chemistry
Bioinformatics students: No


Immune Phenotypes and Breast Cancer Risks
Barbara Fuhrman

CDepartment of Epidemiology, University of Arkansas for Medical Sciences

Dr. Fuhrman’s research focuses on the roles of endocrine and immune factors in the etiology and clinical course of breast cancer.  As a molecular epidemiologist, she designs and carries out studies observational studies of human research participants, who typically undergo research interviews and provide biospecimens for analysis. Two ongoing pilot studies may provide opportunities for student projects, the first of healthy women drawn from the community and the second of women with advanced breast cancer.  Both studies touch a common theme, that the gut microbiome plays a role in breast cancer pathogenesis mediated through its impact on immune response.  These projects can provide experiences in community-based research, epidemiologic field work, laboratory work, data management and data analysis, according to students’ interests, skill set, and willingness to learn.
Prerequisite courses:  Biology and Chemistry
Bioinformatics students:  Yes


Oral Cancer and the Cancer Initiating Cell (CIC) Model in the Context of Tumor Microenvironment and Treatment Resistance

Robert J. Griffin, PhD

Department of Radiation Oncology, University of Arkansas for Medical Sciences

The Griffin lab investigates various aspects of solid tumor biology in the context of response to therapy with radiation, drugs or both. As an example, roughly 35,000 individuals diagnosed with oral squamous cell cancer (OSCC) annually in the U.S (NIDCR statistics) have a 5-year survival rate only slightly above 50%, unchanged over the last decade or more. Complex factors contribute to these dismal statistics: 1) OSCC is usually detected late, when therapies are less effective; 2) even when detected early we lack effective therapies; 3) we also lack reliable prognostic markers of OSCC recurrence, happening in ~25% of the cases. This project will attempt to generate results that might answer the following question: How do we improve the gloomy state of oral cancer management? One answer may lie in the recently proposed CIC model of oral tumorigenesis which, if true, may provide the opportunity for a “paradigm shift” in diagnosis and prevention of oral cancer. In contrast to established thinking (e.g. the clonal evolution model), the CIC model (also known as the cancer stem cell model) proposes that only a sub-set of epithelial cells are responsible for tumorigenesis and eventual tumor progression and spread (metastasis). Furthermore, these CIC cells seem to resist conventional chemoradiotherapy, consistent with ineffectiveness of treatment and recurrence of OSCC observed in the clinic. In line with this idea, we have recently observed that tumor cells growing in contact with endothelial cells as 3D cultures (spheroids) display marked alterations in radiation and chemotherapy sensitivity and, further, have enhanced expression of stem cell markers. This may be dictated by the exchange of microparticles between the cells (called exosomes or microvesicles). Given these results, characterizing CICs, growing in a more realistic 3D environment resembling the perivascular niche where CICs exist in vivo, could provide new information on highly specific and sensitive biomarkers for OSCC early detection and control. Additionally, a “theranostic” approach combining CIC-specific diagnostic biomarkers with customized therapeutic targeting of molecules critical to oral CIC function or viability could revolutionize oral cancer prevention. In this project, advanced in vitro and in vivo tumor cell/endothelial cell models will be used to understand aspects of cell-cell crosstalk (attempting to detect and characterize microvesicles or exosomes) and the stem cell phenotype. A further goal will be to detect/characterize microparticles in circulation that are produced by tumor or normal cells to communicate and orchestrate tumorigenesis.
Pre-requisite courses: Cell Biology and/or Biochemistry, Physiology recommended
Bioinformatics students: Yes


Translational Pharmacogenomics to Improve Drug Safety

Alison H. Harrill, PhD

College of Public Health, Environmental & Occupational Health

The Harrill lab performs research on understanding and predicting adverse drug reactions by identifying genetic variants that influence responses to drugs. To accomplish this goal, a genetically diverse mouse population is utilized to mimic the genetic diversity present in human patient populations. Drugs are administered to the Diversity Outbred mice and biomarkers are measured to determine if the mice experience the relevant clinical drug toxicity. Then, each animal is genotyped using whole genome single nucleotide polymorphism arrays to infer the complete genomic sequence of each animal. Toxicity measurements are then mapped to the mouse genome to identify gene variants that may confer susceptibility to the drug’s toxicity. Additional projects utilize in vitro models to further investigate the relationship between genetic variation and adverse drug responses.


Development of Bioanalytical Methodologies: Tools for the Discovery of New Medications

Howard Hendrickson, PhD

Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences

The Hendrickson lab uses a variety of powerful analytical tools, LC-MS, GC-MS, and NMR to discover clinically relevant biomarkers of disease. Our current interests are on the effects of herbal medicines on the gut metabolome and the effects of ionizing radiation on the biopterin metabolome.

Pre-requisite courses: Freshman Chemistry II

Bioinformatics students: Yes


Food Safety and New Antimicrobial Discovery 

En Huang, PhD
Department of Occuplational Health and Safety, University of Arkansas for Medical Sciences

The main theme of my research is to discover and develop novel antimicrobial peptides (e.g., bacteriocins and lipopeptides). These antimicrobial agents have the potential to be used as natural food preservatives, animal feed additives or novel antibiotics against drug-resistant bacterial pathogens.
Pre-requisite courses: Microbiology lab
Bioinformatics students: Yes


Mechanism of Motor Neuron Degeneration Caused by Mutant Proteins Linked to ALS
Mahmoud Kiaei, PhD 
Department of Pharmacology & Toxicology

The degeneration of motor neurons in brain motor cortex and spinal cord is the main reason for patient with a disease called Motor Neuron Disease (Amyotrophic Lateral Sclerosis) or commonly known in USA as Lou Gehrig’s disease, initially become weak and progress to full paralysis resulting in death. The reasons why motor neurons degenerate and what is/are mechanism(s) is/are not known and is a highly important topic for researchers in the field.

Research in Kiaei laboratory focuses to mimic the disease in the lab using rodents and investigate the disease details in order to learn the mechanisms of neurodegeneration. Recently, Kiaei lab developed a new mouse model for Lou Gehrig’s disease using a newly identified gene linked to the disease, called Profilin1. The first report about this novel model is due to be published in the Journal of Human Molecular Genetics, Fil et al., 2017.

We are exploring this novel mouse model to determine how faulty (mutant) profilin1 protein become toxic to neurons and cause these rodents to develop Lou Gehrig’s disease just like humans? We are interested to investigate profilin1 function (actin binding and polymerization) disruption and how it become toxic to neurons.

Short term projects are available for INBRE students to investigate this very important question of why motor neurons die and how they die that result in human death?  

Pre-requisite course: Biology, Biochemistry
Bioinformatics students: Yes

18UAMS Neurocognitive Dynamics

Linda J. Larson-Prior, PhD
Department of Neurobiology & Developement Sciences


My laboratory is interested in better understanding the dynamic neural network re-configurations that occur as the brain changes its state under both normal conditions such as sleep, and in abnormal conditions such as induced shifts in conscious awareness (anesthesia) or pathological shifts in cognitive awareness (fluctuating consciousness, sleep parasomnias and neurodegenerative disease states).  We have developed the use of simultaneous acquisition of electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) to help us better understand these shifts in network connectivity and function as the brain shifts state over the course of 24 hours. As part of the Human Connectome Project, my laboratory worked with a large international team to define the connection patterns in normal adult human subjects using magnetoencephalography (MEG) and fMRI methodologies.  The connectomics approach to analysis of large, multi-modal datasets is one my laboratory is actively pursuing to better understand the role of behavioral and neural state on function across the lifespan.  I am actively involved in mentoring and mentorship programs and have mentored research professionals at all levels, from high school through early faculty.  In addition, I have provided formal mentorship training to both mentors and mentees through workshops and invited lectures.  I believe strongly that developing strong and proactive mentorship programs early in professional training will aid students in achieving optimal performance levels throughout their careers.
Pre-requisite:  No
Bioinformatics students: Yes


Cellular Mechanisms of Cell Survival and Death
S. Jesse Liu, PhD

Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences

Alterations in membrane transporters and metabolisms by endogenous and exogenous stimuli tilt the balance in cellular mechanisms respectively underlying cell survival and cell death, e.g., during aging and the inflammatory disease. Using multidisciplinary approaches in combination with cultured cells, identification signaling pathways to improve the survival of heart and vascular cells and to facilitate the death of cancer cells would enhance understandings of drug actions and drug development from natural products.
Prerequisites: Biology and Chemistry
Bioinformatics: Yes (optional)


Molecular mechanisms of Intracellular Membrane Trafficking
Vladimir Lupashin, PhD

Departments of Physiology and Biophysics, University of Arkansas for Medical Sciences

The Lupashin laboratory is employing state of the art genetic, cellular and microscopy approached (CRISPR/Cas9-directed gene editing, superresolution microscopy, in vitro reconstruction) to uncover the molecular mechanisms responsible for generation and maintenance of intracellular membrane-bounded compartments in eukaryotic cell. Specifically, we study the machinery that directs docking and fusion of intracellular transport vesicles. The major player of vesicle tethering machinery at the Golgi apparatus is Conserved Oligomeric Golgi (COG) complex. Mutations in COG subunits cause Type II Congenital disorders of glycosylation in humans. COG complex dysfunction in cultured cells results in glycosylation and endo-lysosomal disorders.  We are investigating the molecular mechanisms of COG complex action in different human cell lines.  We also investigating mechanisms that pathogenic microorganisms and toxin use to hijack trafficking compartments in human cells. 
Pre-requisite courses: None
Bioinformatics students:  Yes


Molecular Mechanism(s) of C/EBP delta in Ionizing Radiation Response
Snehalata Pawar, PhD
Division of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences

Dr. Pawar’s research focuses on the role of the transcription factor CCAAT enhancer binding protein (C/EBP) family of transcription factors in ionizing radiation (IR)-induced injury. The overall goal of our research is to understand the molecular mechanisms via which C/EBPs participate in the IR response and to develop novel therapeutic interventions for improved cancer survivorship as well as radiation counter-measure agents. 
Current areas of study in the lab are (i) in vitro and in vivo studies to explore the functional role of C/EBP delta in protection from radiation-induced injury, (ii) identification of upstream regulators of IR-inducible expression of C/EBP delta and (iii) strategies to exploit C/EBP delta as a target to enhance the radiosensitivity of tumor cells and (iv) determine the role of C/EBPdelta in DNA damage response and genomic stability.
The students will be trained to  use a variety of techniques including: molecular biology (PCR), biochemistry (protein expression, Western blots), immunohistochemistry, histology, light/fluorescent microscopy, cell culture techniques, transfections and luciferase reporter assays.
Prerequisites: Chemistry and Biology
Bioinformatics students: Yes


Nitroanisole Detoxification by CYP2E1
Grover Paul Miller, PhD
Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences

Nitroanisoles are environmental pollutants whose toxic potential depends on the efficiency of biological processes.  CYP2E1 likely plays an important role in nitroanisoles metabolism, but the efficiency of the process is unknown.  Kinetic profiling of CYP2E1 activity has been an important tool for assessing the activation and detoxification of many small molecular weight compounds.  Unlike traditional enzymes, CYP2E1 catalysis may involve multiple binding sites that alter the metabolism of compounds.  Recently, we explained unusual non-hyperbolic kinetics for 4-nitrophenol oxidation through the presence of an effector site, which when occupied, suppressed the reaction.  Lack of knowledge of this mechanism could lead to under- or over-estimations of the clearance of compounds from the body.  In the proposed project, we will test the hypothesis that the contribution of P450 enzyme, CYP2E1, to nitroanisole detoxification depends on the occupancy of an effector site by nitroanisoles or the corresponding metabolites.  Through a collaboration between UAMS and Ouachita Baptist University, we will: (1) determine the kinetic mechanisms for nitroanisole metabolism; (2) construct computer models for CYP2E1 complexes with substrates and effectors to predict non-hyperbolic reaction kinetics (Ouachita Baptist University), (3) identify binding site residues for monocyclic molecules through photoaffinity labeling; and (4) confirm functional role for effector site residues through site-directed mutagenesis.  Collectively, these findings will generate models to interpret and predict the efficiency of detoxification of nitroanisoles as well as provide tools for future toxicological studies.  In addition, the combination of biophysical and computational techniques provides an excellent opportunity to cross-train undergraduates and graduate students for successful careers in science. 


UGTs and Nuclear Receptor Activity in Biotransformation of Toxic Compounds
Anna Radominska-Pandya, PhD

Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences

Dr. Radominska-Pandya’s major focus of research is characterization of human UDP-glucuronosyl­transferases (UGTs), enzymes involved in the detoxification of endogenous and exogenous compounds.  She has directed several projects on characterization of UGT cDNAs, proteins, and promoters and is a leader in the area of structure/function relationship studies of UGTs.  Her team has combined chemical, physiological, biochemical, molecular, and computer science approaches to elucidate some of the complex and challenging problems of detoxification reactions that have significant pharmacological and clinical applications.  Currently, the major emphasis of her research is on role of human UGTs in cancer.  These studies are driven by the hypothesis that down-regulation of UGTs could be one of the basic events in neoplastic transformation.  UGTs can metabolize a wide range of carcinogens and could play a critical role in detoxification of these compounds before they can produce carcinogenic effects.  UGTs also are important in conjugating endogenous lipids that are essential for driving cancer cell proliferation. Dr. Radominska-Pandya’s lab has shown that the levels of UGTs in cancer cells, as compared to normal cells, can be significantly altered.  Studies on the reintroduction of suppressed UGTS to tissue culture cells resulted in colony formation, cell growth arrest, and decreased cell proliferation.  Upregulation of specific UGT isoforms is also seen in certain cancer cell lines and is linked to resistance to certain anti-cancer drugs, which can significantly limit the effectiveness of chemotherapy over time.  


Investigating the role of UGTs as anti-proliferative agents in various cancer models

Identifying which UGT isoforms are responsible for resistance to cancer drugs

Delivering UGT genes, siRNA, and/or drugs into cancer cells using nanomaterials as delivery agents

Pre-requisite courses:  None

Bioinformatics students:  Yes


Mechanisms of Action of DNA and RNA Helicases
Kevin D. Raney, PhD
Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences

The Raney laboratory is studying the mechanisms of action of DNA and RNA helicases in work that is funded by the National Institutes of Health. These enzymes manipulate DNA and RNA and enable replication and repair of genomes.  Another project is focused on non-canonical forms of DNA, such as quadruplex DNA.  Biochemical and molecular biological techniques are used for in vitro and cellular experiments. 
Prerequisites: General Chemistry, Organic Chemistry
Bioinformatics student: No


Genetic and Metabolomic Predictors of Longevity and Age-Associated Diseases

Robert J. S. Reis, DPhil

Depts. of Geriatrics and Biochemistry & Molecular Biology at UAMS and the McClellan Veterans Medical Center (CAVHS), University of Arkansas for Medical Sciences

We have an NIH Program Project grant to quantitate metabolite levels and measures of metabolic activity and damage, as well as the status of antioxidant defenses.  We will use these to formulate robust predictors of future longevity in young adults, for a variety of model systems in which life span can be extended markedly by genetic or dietary means.  We will then seek common “fingerprints” indicative of future survival that may extrapolate to humans.  A database will be developed and a variety of means of data mining will be employed to interrogate it.  In the near future, we also plan to develop databases comprising a panel of measures (both those of known clinical prognostic value, and some of the novel markers developed in our model systems), monitored in healthy human subjects.  We can thus look for new markers that correlate well with established biomarkers, and evaluate the application of these metabolic profiles to predicting susceptibility to common diseases and conditions associated with reduced fitness (e.g., obesity, diabetes/impaired glucose tolerance, cancer, high blood pressure, and cardiovascular impairment). 

Pre-requisite courses: None.  Prior courses and/or experience with databases and/or data mining are desirable but not essential.

Bioinformatics students:  Yes


Molecular Mechanisms of Uterine and Mammary Epithelial Cell Growth Regulation
Rosalia C. M. Simmen, PhD  
Department of Physiology and Biophysics, University of Arkansas for Medical Sciences

Studies in the Simmen’s laboratory are focused on two major research areas: 1) elucidation of the molecular mechanisms important for the control of uterine growth and differentiation and its implications on pregnancy and cancer; and 2) the biological consequences of nutrient/gene interactions that might underlie normal development of the mammary gland and initiation and progression of breast cancer in adult life. This research utilizes animal models (rat and mice) as well as human uterine endometrial and mammary carcinoma cell lines and employs a diverse array of molecular, physiological, and cell biological techniques.

Pre-requisite courses: Biology, Inorganic and Organic Chemistry

Bioinformatics students: Yes


Molecular Pathogenesis of Staphylococcus Aureus Musculoskeletal Infection
Mark S. Smeltzer, PhD
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences

Research in the Smeltzer laboratory focuses on Staphylococcus aureus as a musculoskeletal pathogen. We are particularly interested in the surface-exposed adhesions and other virulence factors that allow S. aureus to avoid host defenses and efficiently colonize host tissues and indwelling medical devices, the regulatory circuits that control expression of these virulence factors, and the mechanism(s) by which these factors contribute to the pathology of orthopaedic infections. We are also exploring novel therapeutic methods including the use of nanotechnology as a means of eradicating an established biofilm.  

Pre-requisite courses: Microbiology lab

Bioinformatics students:  Yes


Cellular Mechanisms of Antibody-mediated Immunity against Plasmodium Infection

Jason Stumhofer, PhD
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences

The Stumhofer laboratory studies basic elements of the immune response against the malaria parasite Plasmodium. Using rodent models of infection we are conducting studies to determine the cellular requirements for the development of antibody-mediated protective immunity to Plasmodium. Also, we are interested in determining how and when memory B cells are formed after Plasmodium infection, and their contribution to protection upon secondary infection. Collectively, our studies will provide valuable information regarding the cellular events that contribute to protective immunity against malaria that will be vital for effective vaccine development.

Pre-requisite courses: Microbiology
Bioinformatics students: No



Mechanisms of Intracellular Bacterial Pathogenesis

Daniel E. Voth, PhD

Department of Microbiology & Immunology, University of Arkansas for Medical Sciences

The Voth laboratory is focused on understanding mechanisms used by rickettsial pathogens to parasitize host cells.  Specifically, we are studying Coxiella burnetii, which causes human Q fever, an acute debilitating flu-like illness that also presents as life threatening chronic endocarditis.  We are currently studying host signaling pathways manipulated by Coxiella to generate an intracellular replication compartment with lysosomal features.  Additionally, we are characterizing secreted Coxiella proteins that influence host processes during infection and are predicted to be major virulence factors.  Collectively, our studies will provide new insight into the complex interplay between intracellular bacterial parasites and the host.

Prerequisites:  Cell Biology or Biochemistry

Bioinformatics students:  No


The Platelet Paradigm in Thrombosis, Inflammation and Cancer

Jerry Ware, PhD
Department of Physiology and Biophysics, University of Arkansas for Medical Sciences

The Ware laboratory studies fundamental aspects of platelet biology to elucidate their role of in hemostasis, thrombosis, and inflammation. Since platelets are anucleate fragments of cytoplasm, in vivo models are used based on the hypothesis that the unique cellular characteristics of megakaryocytes and platelets require the correct in vivo environment for meaningful assessment of biological properties. Currently, we are characterizing the platelet’s role in modulating the inflammatory processes associated with sepsis. The clinical management of sepsis remains a challenging and difficult problem and the goal of our work is better understand the complex pathophysiology associated with sepsis.
Pre-requisite courses: None
Bioinformatics students:  Yes


Study of Multiple Myeloma Progression and Bone Metabolism Using Cancer Cells and Animal Models
Donghoon Yoon, PhD
Myeloma Institute, University of Arkansas for Medical Sciences

Multiple myeloma (MM) is a B cell cancer characterized by proliferation of malignant plasma cells in the bone marrow, presence of a monoclonal serum immunoglobulin (non-functional antibodies), and bone lesions. Previous studies demonstrate that bone de-structuring is highly related to Myeloma progression. Our laboratory is studying the effects of various bone forming factors on bone metabolism and MM progression using cell lines and animal models. Trainees in my laboratory will learn cell culture, cell proliferation assays with drug treatment, monitoring drug treated mice and their MM progression using in vivo mouse imaging techniques.
Prerequisite course: Cell biology
Bioinformatics students:  Yes

32UAMS Role of Infant Diet in Gastrointestinal Tract Development and Immune Function
V. Laxmi Yeruva, PhD
Department of Pediatrics, UAMS, ACNC/ACRI

Breastfeeding is known to impart a variety of positive effects on offspring health, including immune system development, and to lower risk for a variety of diseases. Yet, the exact mechanisms underlying these outcomes are not fully known. Research in the Nutritional Immunology group is centered around understanding the early-life events that program gut development, gut microbe ecology and immune function. To address the questions we use a piglet model and a variety of techniques including immunology, immunohistomorphometry, molecular biology (16sRNA sequencing for microbiome, RNA seq analyses), and metabolomics (LC/MS). The big data are analyzed in collaboration with Bio-informatics team at ACNC (Lead by Dr. Brian Piccolo).  Ongoing research seeks to determine the effects of early diet on GI development and function and to what extent these effects are secondary to differences in the gut microbiota, and also immune function. The student interested will be assisting in addressing the short-term goals of our project.
Prerequisite courses: No
Bioinformatics students: Yes








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National Institute of General Medical Sciences (P20 GM103429).

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