The Barouch Lab is focused on defining the peripheral cardiovascular effects of the adipocytokine leptin, which is a key to the understanding of obesity-related cardiovascular disease. Interestingly, many of the hormonal abnormalities seen in obesity are mimicked in heart failure. The research program will enhance the understanding of metabolic signaling in the heart, including the effects of leptin, exercise, sex hormones, and downstream signaling pathways on metabolism and cardiovascular function. The lab also is working to determine the precise role of the “metabolic” beta-3 adrenergic receptor (ß3AR) in the heart and define the extent of its protective effect in obesity and in heart failure, including its role in maintaining nitric oxide synthase (NOS) coupling. Ultimately, this work will enable the exploration of a possible therapeutic role of ß3AR agonists and re-coupling of NOS in preventing adverse ventricular remodeling in obesity and in heart failure. Lili Barouch, MD, is an associate professor of medicine in the Division of Cardiology and a member of the Advanced Heart Failure and Cardiac Transplantation group at the Johns Hopkins University School of Medicine.

The Arking Lab studies the genomics of complex human disease, with the primary goal of identifying and characterizing genetics variants that modify risk for human disease. The group has pioneered the use of genome-wide association studies (GWAS), which allow for an unbiased screen of virtually all common genetic variants in the genome. The lab is currently developing improved GWAS methodology, as well as exploring the integration of additional genome level data (RNA expression, DNA methylation, protein expression) to improve the power to identify specific genetic influences of disease. The Arking Lab is actively involved in researching: • autism, a childhood neuropsychiatric disorder • cardiovascular genomics, with a focus on electrophysiology and sudden cardiac death (SCD) • electrophysiology is the study of the flow of ions in biological tissues Dan E. Arking, PhD, is an associate professor at the McKusick-Nathans Institute of Genetic Medicine and Department of Medicine, Division of Cardiology, Johns Hopkins University.

The goal of the Singh Lab is to cure retinal degeneration due to genetic disease in patients. There are many retinal diseases such as Stargardts, Macular Degeneration, and Retinitis Pigmentosa, that are currently incurable. These diseases damage and eventually eliminate photoreceptors in the retina. The lab's aim is to take healthy photoreceptors derived from stem cells and transplant them into the patient’s retina to replace the lost photoreceptors. The transplanted photoreceptors are left to mature, make connections with the recipient’s remaining retina, and restore vision. Further, the lab is most interested in the cone-photoreceptor rich region of the macula, which is the central zone of the human retina, enabling high-acuity vision for tasks such as facial recognition and reading.

The Johns Hopkins comprehensive Subependymoma and Ependymoma Research Center divideS its efforts into three areas: basic science, translational research and clinical practice. Each division works separately but shares findings and resources openly with each other and our collaborators. The goal of our united efforts is to optimize current treatments to affect the care received by patients with subependymomas and ependymomas. Also, our clinical, translational and basic science teams work to develop novel therapies to improve and extend the lives of those with these rare tumors.

Psychiatric Neuroimaging (PNI) is active in neuropsychiatric research using imaging methods such as MRI, fMRI, PET and DTI to understand the mechanisms and brain networks underlying human cognition. PNI faculty have published hundreds of papers on a variety of brain disorders which include but are not limited to Alzheimer's disease, Parkinson's disease, bipolar disorder, and eating disorders. Faculty in the division have been awarded numerous peer-reviewed grants by the National Institutes of Health, foundations and other funding organizations.

The Amita Gupta Lab focuses on drug trials to prevent and treat HIV, tuberculosis (TB) and other co-morbidities in adults, including pregnant women and children who reside in low-income settings. We also conduct cohort studies assessing HIV, inflammation and nutrition in international settings; TB in pregnancy; and risk factors for TB in India (CTRIUMPH). We collaborate with several faculty in the Center for TB Research, Division of Infectious Diseases and the School of Public Health.

The Advanced Optics Lab uses innovative optical tools, including laser-based nanotechnologies, to understand cell motility and the regulation of cell shape. We pioneered laser-based nanotechnologies, including optical tweezers, nanotracking, and laser-tracking microrheology. Applications range from physics, pharmaceutical delivery by phagocytosis (cell and tissue engineering), bacterial pathogens important in human disease and cell division. Other projects in the lab are related to microscopy, specifically combining fluorescence and electron microscopy to view images of the subcellular structure around proteins.

Brendan Antiochos is a physician scientist in the Division of Rheumatology. His main interest is the role of the innate immune system in the pathogenesis of rheumatic diseases. Current work focuses on the identification of specific endogenous nucleic acids that drive pathogenic innate immune responses in these conditions. More information about his group and work can be found at his lab website.

Our research is focused on understanding the basic mechanisms of programmed cell death in disease pathogenesis. Billions of cells die per day in the human body. Like cell division and differentiation, cell death is also critical for normal development and maintenance of healthy tissues. Apoptosis and other forms of cell death are required for trimming excess, expired and damaged cells. Therefore, many genetically programmed cell suicide pathways have evolved to promote long-term survival of species from yeast to humans. Defective cell death programs cause disease states. Insufficient cell death underlies human cancer and autoimmune disease, while excessive cell death underlies human neurological disorders and aging. Of particular interest to our group are the mechanisms by which Bcl-2 family proteins and other factors regulate programmed cell death, particularly in the nervous system, in cancer and in virus infections. Interestingly, cell death regulators also regulate many other cellular processes prior to a death stimulus, including neuronal activity, mitochondrial dynamics and energetics. We study these unknown mechanisms. We have reported that many insults can trigger cells to activate a cellular death pathway (Nature, 361:739-742, 1993), that several viruses encode proteins to block attempted cell suicide (Proc. Natl. Acad. Sci. 94: 690-694, 1997), that cellular anti-death genes can alter the pathogenesis of virus infections (Nature Med. 5:832-835, 1999) and of genetic diseases (PNAS. 97:13312-7, 2000) reflective of many human disorders. We have shown that anti-apoptotic Bcl-2 family proteins can be converted into killer molecules (Science 278:1966-8, 1997), that Bcl-2 family proteins interact with regulators of caspases and regulators of cell cycle check point activation (Molecular Cell 6:31-40, 2000). In addition, Bcl-2 family proteins have normal physiological roles in regulating mitochondrial fission/fusion and mitochondrial energetics to facilitate neuronal activity in healthy brains.

Research with the Johns Hopkins Division of Reproductive Endocrinology and Infertility (REI) has recently focused on perimenopause and menopause and risks for hot flashes, fertility preservation and on making advances in improving success rates for assisted reproductive technologies. Past research efforts focused on hormonal contraception, prolactin disorders and polycystic ovarian syndrome.