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.
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.
My primary interests concern the effects of environmental toxins, such as lead and PCBs, on oxidative stress and the effects of mitochondrial dysfunction and oxidative stress on radiation-induced normal tissue damage (especially skin and liver).
The lab studies the role of DNases in tissue injury and cell death.
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.
My research focuses on how environmental and occupational exposure, nutrition, and genetic diversity influence cancer initiation, promotion, and progress.
The objective of my laboratory is to develop treatment strategies for opioid use disorder that can be administered to pregnant women without negatively affecting fetuses.
Our primary research interests focus on hemodynamic shear stress, inflammation (e.g. NLRP3 inflammasome and TLR4), mitochondrial DNA damage, programmed cell death (e.g., apoptosis, autophagy, and pyroptosis) and efferocytosis, and their roles in the development of cardiovascular diseases, such as atherosclerosis, myocardial infarction, and aging. Our studies also focus on stem cell therapy, such as use of mesenchymal stem cells and induced pluripotent stem cells, to treat cardiovascular diseases. One of our current studies is trying to computationally integrate state-of-the-art single-cell RNA sequencing (scRNA-seq) with bulk RNA-sequencing and mass spectrometry-driven proteomics to generate a multi-omics whole organ resource of molecular/cellular alterations.
Research in my laboratory is currently focused on several categories of emerging drugs of abuse, including synthetic cannabinoids (constituents of K2/”Spice” smoking blends), analogues of cathinone (present in “bath salts” preparations), and novel arylcyclohexylamines (related to PCP and ketamine.) In an effort to better understand the biological actions of these emerging drugs of abuse, we use behavioral pharmacology techniques in rodents to compare these compounds with more the well-known drugs of abuse that these emerging drugs are designed to mimic (such as the phytocannabinoid delta9-THC, psychostimulants like MDMA and methamphetamine, and PCP).
Our lab studies central nervous system (CNS) injury mainly in the retina and brain. The lab employs different molecular/cell culture techniques, human tissue samples, and animal studies to model critical disease conditions in these two organs. Among the diseases under study are diabetic retinopathy, retinopathy of prematurity, traumatic optic neuropathy, traumatic brain injury, and stroke. Our studies aim to elucidate the underlying pathological mechanisms in these conditions and identify new therapies that can be translated from bench to bedside to help patients affected by these disease conditions.
Dr. Frett's research is focused on small molecule drug design and developing enabling chemical methodologies to expedite the drug discovery process. In particular, he is interested in identifying single-agent therapies capable of controlling multiple, dysregulated pathways in cancer.
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. 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.
Our lab has focused on the novel role of nuclear receptor NR2E3 in liver diseases and cancer. Among 48 human nuclear receptors, the biological roles of NR2E3 remain largely unknown. Our long-term goal is to develop precision medicine for liver disease and cancer based on mechanism-based, gene-oriented epigenetic therapy.
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.
Research interests include drug discovery of targeted therapeutics focusing on Single Agent Poly-pharmacology (SAP), drug discovery research for “non-druggable” targets, and development of a kinase fragment library and novel synthetic methodologies for accelerating the drug discovery process.
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.
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.
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.
Research interests include drug-induced liver injury, biomarkers, liver regeneration, and clinical laboratory testing.
My research group investigates the role of enzymes, especially cytochromes P450 (CYP), in the activation and processing of xenobiotic chemicals, such as drugs, pollutants, and dietary compounds, from a chemist’s perspective. We specialize in the identification and validation of biochemical mechanisms through experimental approaches and often develop analytical tools along the way. Nevertheless, our projects are often multi-disciplinary and collaborative to effectively tackle complex challenges by recruiting experts in computational, analytical, and clinical research.
Research in my laboratory has been and is currently primarily supported by grants from the Veterans Health Administration, National Institutes of Health, and Department of Defense.
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.
The long-term interest of my laboratory is to understand molecular mechanisms responsible for cold storage (CS)-induced renal damage. My research focuses on exploring novel mechanisms by which CS alters protein quality and renal function after transplantation, and importantly, to identify a possible therapeutic target that could lead to improved renal outcome after transplantation. Specifically, I plan to investigate the roles of proteasome, heat shock proteins and complement pathway during CS plus transplantation. We have established a rat kidney transplantation model, which will be fundamental in studying my independent research project on CS mediated renal damage. In addition, I’m also collaborating with Dr. MacMillan-Crow to study the molecular mechanisms that disrupt mitochondrial dynamics during renal CS and transplantation using our rat kidney transplant model.
The overall goal of our research is to develop new antibody-based medications to treat chronic and acute methamphetamine (METH) abuse.
The overall goal of our research program is to better understand the role of the mitochondrion in health and disease. Areas of focus include studying the role of mitochondrial proton leaks in the regulation of metabolic rate, as well as studying the impact of lifestyle (i.e. diet/exercise) and pharmacological interventions on bioenergetics in several settings including developmental programming, obesity and trauma.
We are interested in understanding the mechanisms by which scavenger receptors regulate macrophage function in chronic inflammatory disease.
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.
Dr. Qin's research focuses on cancer oncology and microbiology. He has an active NIH/NCI research award titled Periodontal Bacteria Enhance Oral KSHV Pathogenesis and Kaposi's Sarcoma Development in HIV+ Patients.
My research focuses on the molecular genetics of longevity and age-associated diseases. I was trained in genetics, and turned to C. elegans as a model system in which to define and characterize genes that govern longevity. Using novel gene-mapping methods we developed, we discovered over 27 highly-significant loci for lifespan, resistance to stresses, and Darwinian fitness.
Our research focuses on mechanisms of vascular diseases including hypertension and lymphedema, and therapeutics for these disorders.
Our laboratory is interested in the physiological drivers of colon and breast cancers. Current work in the laboratory and via our collaborations includes: 1) elucidating the role of Krüppel-like factor 9 (KLF9) in cancer suppression; 2) understanding how the hormonal milieu (focus on insulin and the obesogenic environment) affects tumor cell growth; and 3) characterizing the role of Malic Enzyme 1 (ME1) in oncogenesis. Projects use a combination of novel mouse models, human cell lines and tissues, and OMICs technologies and are translational and highly collaborative.
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 interest is focused on learning the techniques and approaches that underscore hypothesis-driven basic and translational cardiovascular/lymphatic pharmacology research. The primary focus is the mechanisms of damage to the lymphatic system during cancer chemotherapy and developing therapeutic strategies to reduce this damage. The laboratory uses techniques such as tissue dissection, enzymatic cell isolation, flow cytometry, vascular functional studies, and gene and protein expression assays. The laboratory also employs both surgical techniques to measure lymph flow in vivo using high-speed optical imaging.
Another area of interest is the potential effects of cardiovascular drugs on lymphatic function. Hypertension has been associated with an increased risk of lymphedema in breast cancer patients. It is unclear whether this increased risk is due to the role of lymphatics in hypertension pathology or the medications used to treat hypertension. Thus we aim to study the effect of antihypertensive agents on lymphatic function and determine the contribution of antihypertensive agents to the development of lymphedema in cancer patients.
Dr. Zhang’s research focuses on cardiac dysfunction in the aging heart with an emphasis on the pathogenic role of elevated proton leak from mitochondria. He explores the strategies of restoring mitochondrial function and stem cell therapies to reverse cardiac dysfunction in preclinical models of aging. Dr. Zhang is the principal investigator of an American Heart Association (AHA) Career Development Award and is an AHA study section member. He has more than 30 original publications and has won several national trainee and junior faculty awards.
Molecular and celllular mechanisms of epilepsy, stroke and other neurological diseases and the discovery of novel therapeutics
I am interested in the role of non-canonical DNA structures and long non-coding RNAs in human disease. I am also interested in clinical applications of microbiome-derived protein biomarkers