Research in the David Sullivan Lab focuses on malaria, including its diagnosis, treatment, molecular biology as it relates to iron, and pathology as it relates to severe anemia. We test and develop new malaria diagnostics — from real-time polymerase chain reaction (PCR) to novel urine and saliva detection platforms. This includes the adaptation of immuno-PCR (antibody coupled to DNA for PCR detection) to malaria and a lead blood stage drug that contains a quinine derivative used to treat malaria in the 1930s.

The goal of the lab's research is to identify molecular abnormalities that can improve the outcome of patients with pancreatic cancer and those at risk of developing this disease. Much of our work is focused on translational research evaluating markers and marker technologies that can help screen patients with an increased risk of developing pancreatic cancer. Thus, marker efforts have been focused mostly on identifying markers of advanced precancerous neoplasia (PanINs and IPMNs) that could improve our ability to effectively screen patients at risk of developing pancreatic cancer. We lead or participate in a number of clinical research protocols involved in the screening and early detection of pancreatic neoplasia including the CAPS clinical trials. We maintain a large repository of specimens from cases and controls with and without pancreatic disease and use this repository to investigate candidate markers of pancreatic cancer for their utility to predict pancreatic cancer risk. In addition, we have been working to identify familial pancreatic cancer susceptibility genes and identified BRCA2 as a pancreatic cancer susceptibility gene in 1996. We participate in the PACGENE consortium and the familial pancreatic cancer sequencing initiative. My lab also investigates pancreatic cancer genetics, epigenetics, molecular pathology, tumor stromal interactions and functional analysis of candidate genes and miRNAs. Dr. Goggins is the principal investigator of a phase I/II clinical trial evaluating the Parp inhibitor, olaparib along with irinotecan and cisplatin for patients with pancreatic cancer.

The Weiss Lab, which features a multi-disciplinary team at Johns Hopkins as well as at Cedars Sinai Medical Center in Los Angeles, is dedicated to identifying the most important clinical, genetic, structural, contractile and metabolic causes of sudden cardiac death as well as the means to reverse the underlying pathology and lower risk. Current projects include research into energy metabolism in human heart failure and creatine kinase metabolism in animal models of heart failure. Robert G. Weiss, MD, is professor of medicine, Radiology and Radiological Science, at the Johns Hopkins University.

The Sfanos Lab studies the cellular and molecular pathology of prostate disease at the Johns Hopkins University School of Medicine. We are specifically interested in agents that may lead to chronic inflammation in the prostate, such as bacterial infections and prostatic concretions called corpora amylacea. Our ongoing studies are aimed at understanding the influence of prostate infections and inflammation on prostate disease including prostate cancer and benign prostatic hyperplasia (BPH). The laboratory also focuses on the influence of the microbiome on prostate disease development, progression, and/or resistance to therapy.

Dr. Raul Chavez-Valdez is an assistant professor in the Department of Pediatrics with great interest in the mechanisms of delayed injury and repair/regeneration in the developing neonatal brain following injury, specifically following hypoxic-ischemic encephalopathy (birth asphyxia). He collaborates with Dr. Frances Northington (Pediatrics) and Dr. Lee Martin (Pathology/Neuroscience) in unveiling the importance of programmed necrosis in the setting of brain injury induced by birth asphyxia. He is especially interested in the role of brain derived neurotrophic factor and neurotrophin-4 following birth asphyxia and the changes that may explain the suspected excitatory/ inhibitory (E/I) imbalance particularly in the hippocampus. His work is highly translational since delayed hippocampal injury due to E/I imbalance may explain memory deficits observed despite therapeutic hypothermia in neonates suffering birth asphyxia. All of these aspects of developmental neuroplasticity are the base of his Career Development Award (NIH/NINDS-K08 award) and applications to other agencies. Additionally, he is part of multiple clinical efforts as part of the Neuroscience Intensive Care Nursery (NICN). He has been a Sutland-Pakula Endowed Fellow of Neonatal Research since September 2013.

The overall goal of the Auditory Brainstem Library is to understand how abnormal auditory input from the ear affects the brainstem, and how the brain in turn affects activity in the ear through efferent feedback loops. Our emphasis is on understanding the effects of different forms of acquired hearing loss (genetic, conductive, noise-induced, age-related, traumatic brain injury-related) and environmental noise. We are particularly interested in plastic changes in the brain that compensate for some aspects of altered auditory input, and how those changes relate to central auditory processing deficits, tinnitus, and hyperacusis. Understanding these changes will help refine therapeutic strategies and identify new targets for treatment. We collaborate with other labs in the Depts. of Otolaryngology, Neuroscience, Neuropathology, the Wilmer Eye Institute, and the Applied Physics Laboratory at Johns Hopkins, in addition to labs outside the university to increase the impact and clinical relevance of our research.