Research in the Howard and Georgeanna Seegar Jones Reproductive Endocrinology Lab supports a broad interest in reproductive conditions, but has a particular focus on endometriosis, uterine fibroids, PMOS and genes causing infertility. PMOS and uterine fibroids are among the most prevalent conditions leading to infertility and diseases in women, but both remain poorly understood. Studying these areas may lead to the development of new treatments or preventative therapies.

The James Laboratory studies mechanisms of bone repair, development, and neoplasia.

The Johns Hopkins Center for Global NCD Research and Training consists of faculty, fellows, and students from institutions across the United States and around the globe. Our mission is to conduct high-quality research and training for the prevention and control of non-communicable diseases in low- and middle-income countries (LMIC), with an aim to build local capacity through partnerships with local institutions and communities. Our current projects encompass subject matters ranging from clean cookstoves to mental health and involve sites in Peru, Uganda, Nepal, and Bangladesh. The burden of NCDs in LMICs is growing rapidly as a result of population aging, rapid unplanned urbanization, and the globalization of unhealthy lifestyles. We envision a robust and sustainable community of NCD researchers and trainees in both high and low income settings dedicated to improving health and well-being for all.

Our research results in effective and quality care which has led to the development of new therapies, medications and vaccines, including the HPV vaccine — the first vaccine to prevent gynecologic cancer. Our patient satisfaction scores are among the highest in the nation, due to our commitment to safety and quality.

Founded in the late 1980s, our Lab explores the fundamental mechanisms of neural responses to traumatic and degenerative signals and works to identify targets for treating injury/degeneration with small molecules, peptides and cells. We currently focus on traumatic and degenerative axonopathies as they occur in traumatic brain injury (diffuse axonal injury), neurodegenerative diseases i.e. Alzheimer's disease and other white matter conditions, e.g. hypoxic ischemic encephalopathy, demyelination. We are especially interested in the role of the MAPK cascade of injury, NAD metabolism and SARM1 signaling and their convergence on Wallerian degeneration.

We are devoted to developing and deploying cutting edge technologies that can be used to define human immune responses. Much of our work leverages ‘next generation’ DNA sequencing, which enables massively parallel molecular measurements. Examples of our technologies include: - bacteriophage display of synthetic peptidome libraries for comprehensive, quantitative profiling of antibodies; - display of ORFeome libraries for antigen discovery, protein-protein interaction studies, and drug target identification; - ultrasensitive, multiplex RNA quantification techniques to monitor gene expression and detect microbes; - pooled genetic screening to elucidate immune cell function and identify new therapeutic targets. The Larman Laboratory uses these and other approaches to identify opportunities for monitoring and manipulating immune responses.

The research conducted in the Mumm Lab (Dept. of Ophthalmology, Wilmer Eye Institute) is focused on understanding how neural circuits are formed, how they function, and how they can be regenerated, to develop new therapies for retinal regeneration. Toward that end, we investigate the development, function, and regeneration of disease-relevant neurons and neural circuits responsible for vision. An emphasis is placed on translating what can be learned in regenerative model systems to develop novel therapies for stimulating dormant regenerative capacities in humans, Therefore, we apply what we learn from a naturally regenerative species, the zebrafish, toward the development of novel therapies for restoring visual function to patients. We place an emphasis on unique perspectives zebrafish afford to biological studies, such as in vivo time-lapse imaging of cellular behaviors and cell-cell interactions, and high-throughput chemical and genetic screening. We have pioneered several technologies to support this work including multicolor imaging of neural circuit formation, a selective cell ablation methodology, and a quantitative high-throughput phenotypic screening platform. Together, these approaches are providing novel insights into how the degeneration and regeneration of discrete retinal cell types is controlled.

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.

The Pathak lab is within the Division of Cancer Imaging Research in the Department of Radiology and Radiological Science. We develop novel imaging methods, computational models and visualization tools to ‘make visible’ critical aspects of cancer, stroke and neurobiology. Our research broadly encompasses the following areas: Functional and Molecular Imaging; Clinical Biomarker Development; Image-based Systems Biology and Visualization and Computational Tools. We are dedicated to mentoring the next generation of imagers, biomedical engineers and visualizers. Additional information can be found at www.pathaklab.org or by emailing Dr. Pathak.

Chronic rhinosinusitis (CRS) is a leading cause of morbidity globally and is the single most common self-reported chronic health condition and accounts for billions of dollars in health care costs and lost work days annually. Exposure to air pollutants is thought to be a critical modifier of CRS susceptibility. Despite marked reductions in air pollution levels in the United States, the fine particulate component of air pollution (PM2.5) and ultrafine pollutants secondary to traffic continue to remain a recalcitrant issue globally and in the United States. The Ramanathan Lab focuses on studying the role of air pollution (PM2.5) in CRS. In collaboration with scientists at the Bloomberg School of Public Health, we have utilized a state of the art air pollution exposure system to develop a novel mouse model of air pollution induced rhinosinusitis that mimics many of the features of CRS in humans. Our lab uses transgenic mouse models and novel immunologic/genomic techniques to study the mechanisms by which PM2.5 causes eosinophilic inflammation and sinonasal epithelial barrier dysfunction. We are also interested in the role of the antioxidant transcription factor, Nrf2, which has shown to stabilize the epithelial barrier and reduce eosinophilia in PM induced rhinosinusitis as a potential therapeutic target.