The Natalie West Lab collaborates with Noah Lechtzin’s lab to study cystic fibrosis, with a particular focus on new resistant bacteria and their effect on the lung function of people with cystic fibrosis.

We investigate the brain networks and neurotransmitters involved in symptoms of movement disorders, such as Parkinson's disease, and the mechanisms by which modulating these networks through electrical stimulation affects these symptoms. We are particularly interested in the mechanisms through which neuromodulation therapies like deep brain stimulation affect non-motor brain functions, such as cognitive function and mood. We use imaging of specific neurotransmitters, such as acetylcholine and dopamine, to understand the changes in brain chemistry associated with the clinical effects of deep brain stimulation and to predict which patients are likely to have changes in non-motor symptoms following DBS. Through collaborations with our neurosurgery colleagues, we explore brain function by making recordings during DBS surgery during motor and non-motor tasks. Dr. Mills collaborates with researchers in the Department of Neurosurgery, the Division of Geriatric and Neuropsychiatry in the Department of Psychiatry and Behavioral Sciences and in the Division of Nuclear Medicine within the Department of Radiology to translate neuroimaging and neurophysiology findings into clinical applications.

The Outcomes After Critical Illness and Surgery Group is focused on understanding and improving patient outcomes after critical illness and surgery. Research projects include improving long-term outcomes research for acute respiratory distress syndrome/acute respiratory failure (ARDS/ARF) patients; examining the long-term outcomes for acute lung injury/acute respiratory distress syndrome (ALI/ARDS) patients; and evaluating the effects of lower tidal volume ventilation and other aspects of critical illness and ICU care on the long-term physical and mental health outcomes of ALI/ARDS patients.

The Fu Lab is a basic research lab that studies zinc transport, with a particular focus on which step in the zinc transport process may be modulated and how. Dr. Fu's lab uses parallel cell biology and proteomic approaches to understand how these physiochemical principles are applied to mammalian zinc transporters and integrated to the physiology of pancreatic beta cells. This research has implications for understanding how zinc transport is related to diabetes and insulin intake.

Research in the laboratory of Felipe Andrade, M.D., Ph.D., focuses on the mechanisms of systemic autoimmune diseases, particularly as they relate to the role of cytotoxic granule proteases in autoimmunity and viral clearance, mechanisms of autoantigen citrullination and pathways that control immune effector functions in autoimmune diseases. We currently focus on two principal areas: (1) defining the mechanisms that generate citrullinated autoantigens in vivo in rheumatoid arthritis and (2) understanding the pathways that control the activity of the peptidylarginine deiminase (PAD) enzymes in human neutrophils.

The Frederick Anokye-Danso Lab investigates the biological pathways at work in the separation of human pluripotent stem cells into adipocytes and pancreatic beta cells. We focus in particular on determinant factors of obesity and metabolic dysfunction, such as the P72R polymorphism of p53. We also conduct research on the reprogramming of somatic cells into pluripotent stem cells using miRNAs.

Research in the Ivor Berkowitz Lab targets pediatric critical care medicine. We are particularly interested in the pathophysiology behind the cerebrovascular dysfunction that occurs in bacterial meningitis as well as the anesthetic and perioperative complications of patients with dwarfing syndromes.

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.

Dr. Faghih is a member of the Johns Hopkins Pancreas Center and is a translational pain researcher who is leading mechanistic studies and clinical trials in chronic pancreatitis-associated pain. One particular aspect of her research is the use of the “Scrambler” device in the treatment of pain from chronic pancreatitis.

The Maryam Jahromi Lab researches infectious diseases such as influenza, tuberculosis, endocarditis, viral hemorrhagic fevers, brucellosis, Clostridium difficile and Crimean-Congo hemorrhagic fever. We are particularly interested in the impact of the influenza vaccine on systemic inflammation. Recent areas of focus include the relationship between influenza vaccination and cardiovascular outcomes, the emergence of Crimean-Congo hemorrhagic fever in Iran, and prospects for vaccines and therapies for Crimean-Congo hemorrhagic fever.