The research in the Svetlana Lutsenko Laboratory is focused on the molecular mechanisms that regulate copper concentration in normal and diseased human cells. Copper is essential for human cell homeostasis. It is required for embryonic development and neuronal function, and the disruption of copper transport in human cells results in severe multisystem disorders, such as Menkes disease and Wilson's disease. To understand the molecular mechanisms of copper homeostasis in normal and diseased human cells, we utilize a multidisciplinary approach involving biochemical and biophysical studies of molecules involved in copper transport, cell biological studies of copper signaling, and analysis of copper-induced pathologies using Wilson's disease gene knock-out mice.

The Seth Blackshaw Lab uses functional genomics and proteomics to rapidly identify the molecular mechanisms that regulate cell specification and survival in both the retina and hypothalamus. We have profiled gene expression in both these tissues, from the start to the end of neurogenesis, characterizing the cellular expression patterns of more than 1,800 differentially expressed transcripts in both tissues. Working together with the lab of Heng Zhu in the Department of Pharmacology, we have also generated a protein microarray comprised of nearly 20,000 unique full-length human proteins, which we use to identify biochemical targets of developmentally important genes of interest.

Current research in the Sean T. Prigge Lab explores the biochemical pathways found in the apicoplast, an essential organelle found in malaria parasites, using a combination of cell biology and genetic, biophysical and biochemical techniques. We are particularly focused on the pathways used for the biosynthesis and modification of fatty acids and associated enzyme cofactors, including pantothenate, lipoic acid, biotin and iron-sulfur clusters. We want to better understand how the cofactors are acquired and used, and whether they are essential for the growth of blood-stage malaria parasites.

Work in the Peter Agre Lab focuses on the molecular makeup of human diseases, particularly malaria, hemolytic anemias and blood group antigens. In 2003, Dr. Agre earned the Nobel Prize in Chemistry for discovering aquaporin water channels. Building on that discovery, our recent research has included studies on the protective role of the brain water channel AQP4 in murine cerebral malaria, as well as defective urinary-concentrating ability as a result of a complete deficiency in aquaporin-1. We also collaborate on scientific training and research efforts with 20 Baltimore-area labs and in field studies in Zambia and Zimbabwe.

The Jean Kim Laboratory performs translational research in the area of chronic rhinosinusitis, with a niche interest in the pathogenesis of hyperplastic nasal polyposis. Studies encompass clinical research to basic wet laboratory research in studying the underlying immune and autoimmune mediated mechanism of polyp growth and perpetuation of disease. Human cell and tissue culture models are used. Techniques in the laboratory include cell and tissue culture, real time PCR, immunoblot, ELISA, flow cytometry, immunohistochemistry, electron microscopy, gene array analysis, and other molecular approaches including genetic knockdowns. Approaches used in Dr. Kim’s clinical study designs include prospective and retrospective analysis of patient outcomes and clinical biomarkers, as wells controlled clinical trials.

Dr. Jantzie, associate professor, received her Ph.D. in Neurochemistry from the University of Alberta in 2008. In 2013 she completed her postdoctoral fellowship in the Department of Neurology at Boston Children's Hospital & Harvard Medical School and became faculty at the University of New Mexico. Dr. Jantzie then joined the faculty Departments of Pediatrics (Neonatal-Perinatal Medicine) and Neurology at Johns Hopkins University and the Kennedy Krieger Institute in January 2019. Her lab investigates the pathophysiology of encephalopathy of prematurity, and pediatric brain injury common to infants and toddlers. Dr. Jantzie is dedicated to understanding disease processes in the developing brain as a means to identifying new therapeutic strategies and treatment targets for perinatal brain injury. Her lab studies neural substrates of cognition and executive function, inhibitory circuit formation, the role of an abnormal intrauterine environment on brain development, mechanisms of neurorepair and microglial activation and polarization. Using a diverse array of clinically relevant techniques such as MRI, cognitive assessment, and biomarker discovery, combined with traditional molecular and cellular biology, the Jantzie lab is on the front lines of translational pediatric neuroscience.?

The Green Group is the biomaterials and drug delivery laboratory in the Biomedical Engineering Department at the Johns Hopkins University School of Medicine. Our broad research interests are in cellular engineering and in nanobiotechnology. We are particularly interested in biomaterials, controlled drug delivery, stem cells, gene therapy, and immunobioengineering. We are working on the chemistry/biology/engineering interface to answer fundamental scientific questions and create innovative technologies and therapeutics that can directly benefit human health.

Research in the Nicola Heller Lab focuses on the immunobiology of macrophages. Our team explores how these cells impact diseases with an inflammatory element, such as cancer, cardiovascular disease and obesity. Using a variety of techniques, including molecular and cellular biology, biochemistry, mouse models and more, we study the role of IL-4/IL-13 signaling in asthma and allergic disease, as well as the role of alternatively activated macrophages (AAM) in the pathogenesis of allergic inflammation. Currently, we are researching the links between asthma and obesity, with a focus on the roles of gender and race.

We investigate the brain networks and neurotransmitters involved in symptoms of movement disorders, such as Parkinson's disease, and the mechanisms by which modulating these networks through electrical stimulation affects these symptoms. We are particularly interested in the mechanisms through which neuromodulation therapies like deep brain stimulation affect non-motor brain functions, such as cognitive function and mood. We use imaging of specific neurotransmitters, such as acetylcholine and dopamine, to understand the changes in brain chemistry associated with the clinical effects of deep brain stimulation and to predict which patients are likely to have changes in non-motor symptoms following DBS. Through collaborations with our neurosurgery colleagues, we explore brain function by making recordings during DBS surgery during motor and non-motor tasks. Dr. Mills collaborates with researchers in the Department of Neurosurgery, the Division of Geriatric and Neuropsychiatry in the Department of Psychiatry and Behavioral Sciences and in the Division of Nuclear Medicine within the Department of Radiology to translate neuroimaging and neurophysiology findings into clinical applications.

In the Lee Martin Laboratory, we are testing the hypothesis that selective vulnerability--the phenomenon in which only certain groups of neurons degenerate in adult onset neurological disorders like amyotrophic lateral sclerosis and Alzheimer's disease--is dictated by brain regional connectivity, mitochondrial function and oxidative stress. We believe it is mediated by excitotoxic cell death resulting from abnormalities in excitatory glutamatergic signal transduction pathways, including glutamate transporters and glutamate receptors as well as their downstream intracellular signaling molecules. We are also investigating the contribution of neuronal/glial apoptosis and necrosis as cell death pathways in animal (including transgenic mice) models of acute and progressive neurodegeneration. We use a variety of anatomical and molecular neurobiological approaches, including neuronal tract-tracing techniques, immunocytochemistry, immunoblotting, antipeptide antibody production, transmission electron microscopy and DNA analysis to determine the precise regional and cellular vulnerabilities and the synaptic and molecular mechanisms that result in selective neuronal degeneration.