The Johns Hopkins Brain Health Program is a multi-specialty team of experts from the Johns Hopkins School of Medicine, Whiting School of Engineering, and the Bloomberg School of Public Health.

Dr. Wu leads a multi-disciplinary team with collaborators from the Bloomberg School of Public Health, JHU Whiting School of Engineering, and JHU Krieger School of Arts and Sciences. She conducts ongoing investigations with the Multicenter AIDS Cohort Study and Women’s Inter-agency Health Study. Her lab’s goals are to develop, implement, and validate novel imaging-based metrics of cardiac structure and function to improve risk prediction and stratification at the individual patient-level. Research Focuses: Predictors of Sudden Cardiac Death by Magnetic Resonance Imaging Subclinical myocardial disease in people living with HIV Individualized risk prediction Cardiac structural and mechanical modeling

The Konig Lab focuses on chimeric T cell- and antibody-based strategies for the treatment of autoimmune rheumatic diseases and cancer. A primary goal of the translational research program is the development of antigen-specific and personalized immunotherapies for autoimmune diseases, with the intent to achieve sustained disease remission and functional cure. The lab further aims to establish precision T cell-targeting therapies for the treatment of various autoimmune diseases. Applying these tools to immuno-oncology, the lab utilizes cellular engineering strategies to augment the cytotoxic killing of solid cancers by the immune system.

Our group is interested in a broad array of clinical and translational investigations spanning the evaluation of basic pathophysiology in patients undergoing cardiac procedures, development and evaluation of new therapeutic strategies, and improving patient selection and outcomes following interventional procedures. We are comprised of a core group of faculty and dedicated research nurses as well as fellows, residents, and students. Projects range from investigator-initiated single-center observational studies to industry-sponsored multicenter phase 3 randomized controlled trials. We have established a database of all patients who have undergone TAVR at Johns Hopkins, which is providing the basis for several retrospective analyses and will serve as the foundation for future studies of TAVR. We are also engaged in collaborative projects with other groups from the Department of Medicine and other Departments including Cardiac Surgery, Anesthesiology, Radiology, Psychiatry, and Biomedical Engineering. Members of our group are actively involved with the Johns Hopkins Center for Bioengineering Innovation and Design (CBID) in the development of novel minimally-invasive cardiovascular devices.

Complexity in signaling networks is often derived from co-opting one set of molecules for multiple operations. Understanding how cells achieve such sophisticated processing using a finite set of molecules within a confined space--what we call the ""signaling paradox""--is critical to biology and engineering as well as the emerging field of synthetic biology. In the Inoue Lab, we have recently developed a series of chemical-molecular tools that allow for inducible, quick-onset and specific perturbation of various signaling molecules. Using this novel technique in conjunction with fluorescence imaging, microfabricated devices, quantitative analysis and computational modeling, we are dissecting intricate signaling networks. In particular, we investigate positive-feedback mechanisms underlying the initiation of neutrophil chemotaxis (known as symmetry breaking), as well as spatio-temporally compartmentalized signaling of Ras and membrane lipids such as phosphoinositides. In parallel, we also try to understand how cell morphology affects biochemical pathways inside cells. Ultimately, we will generate completely orthogonal machinery in cells to achieve existing, as well as novel, cellular functions. Our synthetic, multidisciplinary approach will elucidate the signaling paradox created by nature.

The Division of Maternal-Fetal Medicine is engaged in clinical, basic bench and epidemiological research as one of its primary missions. Our strength lies in the expertise and diverse interests of our faculty, as well as in the collaborations with multiple other disciplines and departments throughout the School of Medicine, The Bloomberg School of Public Health, and the School of Biomedical Engineering. The strong research infrastructure of the Johns Hopkins University forms a solid foundation for the success of our integrated research program for Maternal-Fetal Medicine.

Epilepsy affects 1-3% of the population and can have a profound impact on general health, employment and quality of life. Medial temporal lobe epilepsy (MTLE) develops in some patients following head injury or repeated febrile seizures. Those affected may first suffer spontaneous seizures many years after the initial insult, indicating that the neural circuit undergoes a slow pathologic remodeling over the interim. There are currently no methods of preventing the development of MTLE. It is our goal to better understand the process in order to slow, halt, and ultimately reverse it. Our laboratory draws on electrophysiology, molecular biology, and morphology to study the contribution of dysregulated neurogenesis and newborn neuron connectivity to the development of MTLE. We build on basic research in stem cell biology, hippocampal development, and synaptic plasticity. We work closely with colleagues in the Institute for Cell Engineering, Neurology, Neurosurgery, Biomedical Engineering, and Radiology. As physician neuropathologists our grounding is in tissue alterations underlying human neurologic disease; using human iPSC-derived neurons and surgical specimens we focus on the pathophysiological processes as they occur in patients. By understanding changes in cell populations and morphologies that affect the circuit, and identifying pathologic alterations in gene expression that lead to the cell-level abnormalities, we hope to find treatment targets that can prevent the remodeling and break the feedback loop of abnormal activity > circuit change > abnormal activity.

Five to 35 percent of spine fusionprocedures fail, even when using the gold standard treatment of grafting bone from the patient's own iliac crest. Fusion failure, otherwise known as pseudoarthrosis, is a major cause of failed back surgery syndrome (FBSS) and results in significant pain and disability, increasing the need for additional procedures and driving up health care costs. The ultimate goal of the Spinal Fusion Laboratory is to eliminate pseudoarthrosis by using animal models to study various strategies for improving spinal fusion outcomes, including delivery of various growth factors and biological agents; stem cell therapies and tissue engineering approaches.