Dr. Sohn's lab is interested in understanding how biological stress-sensors are assembled, detect danger signals and initiate stress response. Innate immunity is the first line of defense against invading pathogens in higher eukaryotes. We are using in vitro quantitative biochemical assays and mutagenesis and x-ray crystallography to investigate the underlying operating principles of inflammasomes, a component of the innate immune system, to better understand biological stress sensors.

Research in the Justin Bailey Lab explores immune responses against hepatitis C virus (HCV), particularly neutralizing antibody responses, with the goal of guiding vaccine development against the virus. Recent studies have demonstrated that early and broad neutralizing antibody (nAb) responses against HCV are associated with HCV clearance, suggesting a key role for nAb in limiting HCV replication. The findings of this research will enhance understanding of how HIV infection may contribute to the lower rate of HCV clearance in HCV/HIV coinfected individuals, and the results could have implications for persistence of other viruses commonly occurring as coinfections with HIV.

The Kalina Hristova Lab investigates the structure and assembly of biological membranes. Our team conducts research on the structural and thermodynamic principles that enable membrane protein folding and signal transduction across biological membranes. Part of our work has involved developing new tools to study the structure of thermally disordered fluid membranes and the energetics of biomolecular interactions in biological membranes. Through our studies, we have established a better understanding of the physical principles behind complex biological processes and the mechanisms of disease development in humans.

The Karakousis Lab is primarily focused on understanding the molecular basis of Mycobacterium tuberculosis persistence and antibiotic tolerance. A systems biology-based approach, including the use of several novel in vitro and animal models, in combination with transcriptional, proteomic, genetic, imaging, and computational techniques, is being used to identify host cytokine networks responsible for immunological control of M. tuberculosis growth, as well as M. tuberculosis regulatory and metabolic pathways required for bacillary growth restriction and reactivation. In particular, we are actively investigating the regulatory cascade involved in the mycobacterial stringent response. Another major focus of the lab is the development of host-directed therapies for TB, with the goal of shortening treatment and improving long-term lung function. Additional research interests include the development of novel molecular assays for the rapid diagnosis of latent TB infection and active TB disease, and for the detection of drug resistance.

The Karen Bandeen-Roche Lab explores the application of underlying variable methods in epidemiologic and psychosocial research. Our team seeks to improve the ability to measure key outcomes like functional status and psychological disorders. Our other areas of statistical research include the study of classification and variance structure and multivariate survival analysis. We are deeply invested in the field of gerontology as well as ophthalmology and neurology.

The focus of the research in the Reddy Laboratory is to begin to understand how the nuclear periphery and other subcompartments contribute to general nuclear architecture and to specific gene regulation. Our research goals can be broken down into three complementary areas of research: understanding how genes are regulated at the nuclear periphery, deciphering how genes are localized (or ""addressed"") to specific nuclear compartments and how these processes are utilized in development and corrupted in disease.

Dr. Amir Kashani and his team are developing novel diagnostic and therapeutic methods to diagnose and treat retinal diseases using advanced imaging methods. These methods can detect the earliest changes in retinal capillaries before they are noticeable to the patient or doctor.

Basic science investigations span an array of inquiries, such as understanding the basic mechanisms underlying cardiac dyssynchrony and resynchronization in the failing heart, and beneficial influences of nitric oxide/cGMP/protein kinase G and cGMP-targeted phosphdiesterase signaling cascades on cardiac maladaptive stress remodeling. Recently, the latter has particularly focused on the role of phosphodiesterase type 5 and its pharmacologic inhibitors (e.g. sildenafi, Viagra®), on myocyte signaling cascades modulated by protein kinase G, and on the nitric oxide synthase dysregulation coupled with oxidant stress. The lab also conducts clinical research and is presently exploring new treatments for heart failure with a preserved ejection fraction, studying ventricular-arterial interaction and its role in adverse heart-vessel coupling in left heart failure and pulmonary hypertension, and testing new drug, device, and cell therapies for heart disease. A major theme has been with the use of advanced non-invasive and invasive catheterization-based methods to assess cardiac mechanics in patients.asive and invasive catheterization-based methods to assess cardiac mechanics in patients. David Kass, MD, is currently the Director at the Johns Hopkins Center for Molecular Cardiobiology and a professor in cellular and molecular medicine.

We started Kata to bridge the gap between professional experiential production and neuroscience, clinical neurology, and medical hardware. We strive to build experiences and technology from the ground up, with a focus on mission, and at a level that is consistent with the best productions in the industry. We mirror the thousands of hours that go into a level design in a video game, but with the crucial difference that the focus is on the subtleties required for patient treatment or wellness. Our designs require high-frequency iterative development with patients and users in countless game-play sessions in which they provide crucial feedback. Characters have been painstakingly crafted to elicit profound emotional responses. Some of the requirements for patients or the elderly population in this space are qualitatively different from what is needed in the entertainment marketplace. That said we have also understood the critical artistic similarities. The core ethos of Kata is that the challenge of complex movement has profound benefits for cognition, wellness, and brain repair. Specifically, there is growing evidence that complex motor movement can have cognitive benefits that go beyond what has been reported for exercise alone. When designing experiences to treat motor impairments after stroke, maximizing rigorous and dynamic motor input is a requirement. New interactive technologies will allow people to engage in diverse and complex motor movements, even in the home, which was previously impossible. Overall it has been a very exciting journey, combining art, medicine, technology, and neuroscience. We continue to build, discover, and craft immersive experiences, side by side with physicians, physical therapists, and scientists, with the common goal of pushing clinical care and wellness forward. We believe this is only possible by having a mission focused design group embedded in an academic hospital. Ultimately, we wish to scale and perfect these innovations into other hospitals. Kata is a true hybrid of academia, and industry, doing what neither can do in isolation. We hope the ethos and design philosophy behind Kata provides the impetus for its expansion, partnerships, and growth.

Research in the Wilson Lab focuses on three components of nuclear lamina structure: lamins, LEM-domain proteins (emerin), and BAF. These three proteins all bind each other directly, and are collectively required to organize and regulate chromatin, efficiently segregate chromosomes and rebuild nuclear structure after mitosis. Mutations in one or more of these proteins cause a variety of diseases including Emery-Dreifuss muscular dystrophy (EDMD), cardiomyopathy, lipodystrophy and diabetes, and accelerated aging. We are examining emerin's role in mechanotransduction, how emerin and lamin A are regulated, and whether misregulation contributes to disease.