Our laboratory utilizes pharmacologic approaches and genetic models to examine how the changes in the neuronal microenvironment e.g. inflammation, oxidative stress affects cognitive function.
Dr. Allen's lab uses informatics, high-throughput sequencing, in vitro, ex vivo, and in vivo models to study the link between lipoproteins and inflammation in cardio-metabolic disease.
Our research investigates the effects of nutrition, body composition and physical activity on growth and metabolism of infants and children. Our multi-disciplinary group addresses complex questions regarding the interaction of these variables while considering multiple facets of child development. Major research projects currently investigate the consequences of prenatal environment and early infant feeding. Other projects also examine how to optimize nutrition and physical activity to improve overall health.
I am a physician-scientist with research and clinical interests in the prediction of outcomes in kidney disease. The research in my laboratory focuses on the discovery and validation of biomarkers in renal diseases including acute kidney injury, diabetic nephropathy, chronic kidney disease and glomerular diseases like IgA nephropathy. We use targeted analysis of candidate markers by multiplexed bead array, ELISA and mass spectrometry and proteomic discovery analyses by liquid chromatography/mass spectrometry to identify and qualify biomarkers in animal models and humans.
Our lab studies the characteristics and regulation of cell states in health and disease. We use human induced pluripotent stem cells (iPSCs), intact human and mouse tissues, pre-clinical rodent models and omics platforms to understand the molecular pathways that drive cellular plasticity in cardiovascular and metabolic diseases. We also employ genetic and pharmacological manipulations in cells and mice to investigate how specific genes/proteins may cause cell state transitions, thereby contributing to cardiometabolic diseases.
My research focuses on Melanocortin-4 receptor, a G-protein coupled receptor involved in appetite control.
My lab is focused on Alzheimer’s disease. Current research is examining the role of diabetes-related disruptions in glucose metabolism and the impact this has on brain function. Evidence indicates that both Alzheimer’s and diabetes involve processes connected to inflammation, which has been another of my longstanding areas of research.
The lab studies the role of DNases in tissue injury and cell death.
The Bellido laboratory investigates the mechanisms of signal transduction among and within bone cells, with particular emphasis on the biology of osteocytes, and in cells of skeletal muscle. The laboratory employs in vitro, ex vivo and in vivo models to study how hormones and mechanical force act on bone and muscle cells and affect their function.
The overall objective of my research is to elucidate biological mechanisms of cardiovascular injury from exposure to ionizing radiation and to identify potential methods for intervention. We focus on radiation-induced heart disease as a side effect of radiation therapy to the chest and cardiovascular effects of exposure to space radiation. Our research is performed with animal models of whole-body irradiation and image-guided localized irradiation combined with in vivo non-invasive echocardiography, ex vivo cardiac function measurements, and histological and molecular analyses.
The overall aim of our program is to promote life-long health starting from the very beginning of a human’s life. Specifically, our research program is focused on studying the effects of physical activity, alone and in combination with nutrition, on optimal growth and development of children, including underlying biological mechanisms. We seek to understand the mechanistic consequences of inactivity and suboptimal nutrition on obesity and related metabolic disorders, and also how maternal physical activity during fetal development (i.e., training during pregnancy) and physical activity during childhood can prevent and/or reverse these conditions.
Dr. Carroll is a researcher at Arkansas Children’s research Institute (ACRI). Dr. Carroll’s research interests include posnatal maturation of oxygen sensing, pediatric sleep apnea, respiratory control maturation, postnatal chemoreceptor development, effects of hyperoxia, chronic hypoxia and chronic intermittent hypoxia on respiratory control maturation, childhood sleep disordered breathing, chronic lung disease of prematurity, long-term ventilation and the respiratory care of medically complex children with respiratory technology-dependence.
We are actively studying the role of leptin in the regulation of pituitary cells. We have discovered that leptin may be a post transcriptional regulator for target hormones, receptors and transcription factors. Our studies range from whole animal to molecular approaches and a student would get training in a number of complementary protocols. Our studies are translationally relevant to growth, obesity, reproduction, and fetal and neonatal development.
Our research focus is aimed at investigating the epigenetic regulatory mechanisms at the enhancers and promoters of the critical oncogenes and tumor suppressors that drive malignant proliferation and invasion during leukemogenesis in the Acute Myeloid Leukemia (AML) patients, characterized with BET (BRD4), SET (KMT2A, EZH2, and NSD1) or runt (CBFA2T3) over-expressed domains. Using the multi-omics platform, we intend to identify the alterations in DNA methylation, histone modifications and transcription factor assemblies in and outside the topologically assorted domains (TAD) in AML. We also aim to study the recurrent epigenetic mutations in AML patients in relation to their effect on the cancer cell metabolism. Suitable cells or animals will be induced with the mutant proteins to study the deleterious effects on the chromatin spread, transcriptional dysfunctions and metabolic turnover in the course hematopoiesis. CRISPR-multiplex or small molecule based drugs would be screened for their efficacy against the vulnerable targets of the mutant phenotypes
Dr. Cornett’s research interests are focused primarily on the homeostatic roles of the neurohypophysial hormone vasotocin in the domestic chicken and secondarily on the regulation of adrenergic receptor gene expression in mammals. Regarding the actions of vasotocin, immunohistochemical techniques, radioimmunoassays and in situ hybridization histochemistry are used to investigate the regulation of vasotocin gene expression in the chicken hypothalamus under conditions of osmotic stress and during oviposition.
The Delgado-Calle laboratory focuses on understanding the mechanisms by which cancer cells alter the biology of other cells in the tumor/bone marrow microenvironment, in particular osteocytes, with the final goal of identifying targetable factors for the treatment of cancer that grows in bone. We employ ex vivo and in vitro models to study osteocyte-tumor biology, and animal models of cancer-induced bone disease to characterize the effects of genetic and pharmacologic approaches on tumor growth and bone remodeling. Current projects in the laboratory investigate the effects osteocyte-derived factors and bidirectional Notch signaling between myeloma cells and osteocytes on MM progression, myeloma cell dormancy, and cancer-induced bone disease.
The lab studies the structure and function of carbohydrate-binding proteins in prostate cancer and reproduction.
The Dole laboratory primarily focuses on how obesity and loss of body weight impact bone health and contribute to skeletal etiologies like osteoporosis and osteoarthritis. The current studies of the group cover three major themes: 1. The interplay of early-life factors, including prenatal and postnatal nutrition, on the development and maintenance of the skeleton; 2. Epigenetic and molecular biomarkers associated with obesity and weight loss in bone; 3. Role of mitochondrial energetics in skeletal and extraskeletal functions of bone (mineral and whole-body energy metabolism). Our ultimate goal is to leverage bone as a therapeutic target to lessen the burden of chronic metabolic diseases and improve physical function and quality of life.
Dr. Drew conducts research in the field of Neuroimmunology. Normally, immune activity in the brain is limited. However, in diseases including multiple sclerosis, Alzheimer’s disease, and alcohol abuse activated immune cells are observed in the brain. These immune cells produce cytokines which may be toxic to brain cells as well as chemokines which direct cells to sites of inflammation, resulting in neuropathology. Dr. Drew’s research involves modern cellular and molecular biology techniques.
Virology, cancer biology, immunology! Gammaherpesviruses 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. Our major goal is to comprehend the complex relationship between gammaherpesviruses and their hosts. PLUS, we get to do cool science and figure out how stuff works!
Radiation and Cancer biology, exosomes and cell to cell crosstalk in stem cell differentiation and activity, nanomedicine applications. Dr. Griffin’s research interests include: molecular and physiological mechanisms of radiation and thermal sensitization; modulation of tumor blood flow, angiogenesis and oxygenation; biology and physiology of thermal therapy; and oxygen partial pressure as predictor of cancer treatment response.
Dr. Griffin focuses on the mechanisms involved in the progression of Alzheimer’s disease and other neurodegenerative conditions such as Parkinson’s disease, Down Syndrome, head trauma, and epilepsy.
Electrophysiology of olfactory bulb and cerebellar neurons - Alcohol research - Rhythmic motor movements such as licking and running - Effects of radiation on neuronal function - Imaging neuronal network - Synchronous bursting of neurons.
Dr. Ho's research interests pertain to the role of hormones and endocrine disruptors, and the interplay between genetics and epigenetics, in disease development as well as how early-life experiences can be a root cause in later development of cancers, asthma, neural disorders and other complex chronic diseases.
My laboratory studies lung macrophages and their roles during the infection of Mycobacterium tuberculosis. We aim to understand the ontogeny of lung macrophages and how different metabolic pathways regulate their functions in tuberculosis. In addition, we are particularly interested in the crosstalk between cellular metabolism and epigenetic regulation in lung macrophages.
I study the structure and function of membrane proteins that transport ions, with emphasis on coupled exchangers and cotransporters. Experimental systems include red blood cells, yeast, and cultured mammalian cells,
Dr. Jones research focuses on both clinical and translational investigation of food allergy and eosinophilic gastrointestinal disorders, in particular in finding new therapies and improving understanding of disease. Dr. Jones also has a long-standing research interest in asthma and lung disease.
Cancer vaccine and immunotherapy; Tumor glycans; Tumor progression and metastasis; Cancer and metabolism.
Dr. Kim has worked on several projects investigating age-related bone loss. He also discovered that anti-aging FoxO transcription factors restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation. His recent work led to the seminal finding that cellular senescence of osteoprogenitors and osteocytes causes age-related bone loss. The skills and knowledge were acquired during his research on bone metabolism and have laid the foundation for him to begin his work as a junior faculty member in the Division of Endocrinology.
Dr. Leung is an established investigator in the field of hormone regulation of cancer and is an expert on the developmental origin of cancer risk and the impact of environmental estrogens/endocrine disruption on epigenetics reprogramming.
The Liu lab studies host intrinsic innate signaling using poxvirus as probing tool. We also engineer poxviruses for immunotherapy of cancer such as ovarian cancer.
My laboratory is interested in understanding the molecular mechanisms responsible for the generation and maintenance of intra-cellular membrane-bounded compartments. In all eukaryotic cells intracellular membrane trafficking is critical for a range of important cellular functions including protein secretion, post-translational modifications, cell signalling, cell polarization, and cell maintenance. Defects in membrane trafficking can underline, or even exacerbate, a number of human diseases including cancer, diabetes mellitus, Alzheimer’s, cystic fibrosis, Hermansky-Pudlak syndrome and Congenital Disorders of Glycosylation.
Elucidation of biochemical mechanisms involved with kidney damage during sepsis and transplantation. Focus on mitochondria, cell death, and oxidant generation as well as novel therapies to reduce damage.
My research focuses on cell cycle control, stem cells, cancer stem cells, drug discovery, mRNA translation, and vertebrate development.
I am working on identification of the cellular mechanisms that control cell growth and development. I am particularly interested in the role and regulation of stem cells in neural development and in cancer.
Not accepting students as a major advisor
We are interested in studying primary effusion lymphoma (PEL), an aggressive B cell cancer caused by the Kaposi’s sarcoma-associated herpesvirus or human herpesvirus 8 (KSHV/HHV8). PEL tumor cells rely on the constitutive expression of virally encoded genes that globally reprogram host gene expression to create a conducive environment optimal for tumor cell proliferation and survival.
Molecular biology; adipocyte development; regulation of adipogenesis by retinoblastoma proteins.
Research interests include drug-induced liver injury, biomarkers, liver regeneration, and clinical laboratory testing.
Dr. Mehta is a Distinguished Professor of Medicine, and Physiology and Biophysics, and the Stebbins Chair in Cardiology at UAMS.
We utilize genetically modified mouse models to understand the function of poorly characterized genes that have a function in skeletal development, homeostasis or disease. A special interest is in proteins that post-translationally modify collagens and in osteogenesis imperfecta.
The primary interest of my research has been focusing on the pathogenesis of hypertension in renal salt-reabsorption and the systemic vasculature. The long-term goal of our laboratory is to understand the mechanism of the development of hypertension and to translate our basic scientific discovery to clinics to contribute to a final cure for hypertension.
My research focuses on the area of applied bioinformatics/computational biology and systems biology for biomedical research. I have developed novel advanced algorithms and frameworks to accelerate the utilization and mining for biological interpretation of omics data (genome, transcriptome, proteome and metabolome) for biomedical research translation (cancer, obesity, diabetes, autoimmune disease, metabolic dysfunction, etc.). In addition, I also focus on the impact of human gut microbiome on diseases progression and development.
We want to understand the cellular and molecular mechanisms that cause bone loss with aging, estrogen-deficiency, and glucocorticoid excess.
Our laboratory is interested in autophagy in osteoblast lineage cells in efforts to understand the role of autophagy in bone remodeling and age-related bone loss.
Research interests include new quantitative MRI methods and effects of nutrition/obesity on brain development in children.
Dr. Pathak’s current research interest is radiation-induced normal tissue injury particularly radiation-induced endothelial dysfunction and genomic instability using FISH-based molecular techniques.
Research areas of interest and expertise include: regenerative medicine, anterior cruciate ligament, articular cartilage, molecular imaging, mesenchymal stem cell, gene therapy, chondrocytes, cartilage repair, and preclinical models.
I am a cellular/molecular pharmacologist whose research interests involve understanding the neurobiological mechanisms underlying the addictive states produced by drugs of abuse. Specifically, for over 20 years I have been investigating the cellular and molecular mechanisms of signal transduction mediated by G-protein coupled receptors (GPCRs) with which drugs of abuse interact, specifically opioids and cannabinoids.
The Sato Laboratory investigates mechanisms by which excessive GC induce disease in the musculoskeletal and cardiac systems with the overall goal of identifying novel targets for therapeutic intervention in the context of GC with and without a primary affliction, such as Duchenne Muscular Dystrophy.
The overall goal of my research is to elucidate the role of stress-induced molecular pathways on the skeletal effects of sex steroid deficiency and old age. Our work combines the use of genetic and pharmacological approaches in mice, with biochemical and molecular testing in cultured bone cells, to discover critical pathophysiological mechanisms and potential anti-osteoporotic therapies.
My research is focused on defining the mechanisms underlying the dynamics and combinatorial relationships of regulatory pathways implicated in the biology and pathobiology of the mammary gland and the uterus. We have a specific interest in elucidating the signaling pathways by which steroid hormone receptors, growth factors, cytokines and dietary components are engaged in the pathogenesis of breast cancer and uterine-associated diseases. We employ diverse cellular and molecular techniques and experimental models including gene arrays for gene discovery, cell lines for analyses of signaling pathways, and human and mouse models of diseases to address basic goals with translational potential.
The activity of primary sensory neurons is critical for the development and maintenance of persistent pain states. Following peripheral injury, primary sensory neurons show complex activity-dependent plasticity as a result of prolonged noxious stimuli and ectopic discharges. This altered activity in the primary sensory neurons is transmitted to spinal dorsal horn neurons and ultimately to the brain which results in persistent pain in a proportion of patients. While genetic studies have advanced our knowledge of nociceptive pathways, our current understanding does not explain variations in the susceptibility of individuals to the development of this cancer-related persistent pain. Common genetic variations in pain phenotypes show inconsistencies across studies6 and have not facilitated the development of new treatments. Epigenetic variations within the genome are known to cause misregulation of protein at a cellular level which may modulate nociception. My long term goal is to determine the contribution of epigenetic pathways to enhanced pain sensitivity and the establishment of cancer-related persistent pain. Specific research questions that I am eager to explore include (1) the association between altered chromatin structure in the dorsal root ganglion and cancer-related pain, and (2) cell-type specific changes in chromatin accessibility associated with chemotherapy-induced peripheral neuropathy.
My research focuses on organelles of the secretory pathway using HeLa cells as an easy cell for molecular manipulations of the Golgi apparatus and platelets as structure/function example of a stored secretory granules.
We are using ‘third generation sequencing technology’ (such as Oxford Nanopore flow cells) to do metagenomics of clinical isolates and environmental samples.
The Voth laboratory uses novel human-derived models of infection to study bacterial pathogens that establish pulmonary infections in humans.
My research focuses on chromosome dynamics, epigenetics, cellular growth controls.
My research focuses on the role of circulating blood platelets, in thrombosis, inflammation, and cancer
According to the CDC, more than 1 billion people, or one-sixth of the world’s population, is suffering from one or more Neglected Tropical Diseases with many of these diseases affecting the poorest populations in the developing world. Our lab focuses on the parasitic disease that results from Leishmania infection. We use a combination of mouse models and in vitro culture to define the cellular and molecular mechanisms that are important in the development of disease and the resolution of inflammation. More specifically, we are interested in the balance between the vascular and immune responses that lead to parasite control and those that promote lesion pathology.
The focus of research in my laboratory is centered on CNS development, particularly with regard to the formation and maintenance of myelin.
Dr. Yaccoby research focuses on pathogenesis of multiple myeloma, tumor microenvironment, bone marrow mesenchymal stem cells, and tumor initiating cells.
Our lab focus on two aspects 1. Role of Chlamydia variants in host pathogenesis. 2. Role of infant diet in gastrointestinal tract development and immune function.
We are interested in the pathophysiology of multiple myeloma (MM), a B cell cancer characterized by proliferation of malignant plasma cells in the bone marrow, presence of a monoclonal serum immunoglobulin, and osteolytic lesions. We are investigating roles/mechanisms of PTH axis (PTH signal transduction) in MM development and therapeutic agents that target this axis. Additionally we are exploring the roles of Hypoxia (low oxygen tension) and microRNA (miRNA) in MM.
Molecular and celllular mechanisms of epilepsy, stroke and other neurological diseases and the discovery of novel therapeutics