Duke Anesthesiology’s world-class team of researchers is devoted to preclinical studies that can lead to critical discoveries, ultimately advancing patient care. Basic science researchers generate new concepts and theories to form the basis of progress and development in a variety of fields. Our department is committed to research that focuses on mechanisms of chronic pain, a common affliction requiring breakthrough science to transform the way we provide care for patients. Our researchers work in independent yet collaborative laboratories, and co-investigate with multiple disciplines within and outside of Duke University Medical Center.
Learn about each of the 10 research laboratories in the Department of Anesthesiology
- Chemical Sensing, Pain and Inflammation Research Laboratory
- FG Hall Environmental Laboratory
- Molecular Neurobiology Laboratory
- Multidisciplinary Neuroprotection Laboratory
- Molecular Pharmacology Laboratory
- Nerve Injury and Pain Mechanism Laboratory
- Neuroinflammation and Cognitive Outcomes Laboratory
- Pain Signaling and Plasticity Laboratory
- Systems Modeling of Perioperative Cardiovascular Injury and Adaptation Laboratory
- The Nackley Lab
Research in the Chemical Sensing, Pain and Inflammation Research Laboratory focuses on the mechanisms that enable humans and animals to sense touch, pain and irritation. These fundamental sensations originate in peripheral sensory neurons, which contain signaling pathways that translate environmental, physical and chemical stimuli into neural activity.
The FG Hall Environmental Laboratory is dedicated to the investigation of hypoxia, hyperoxia, low and high ambient pressures, immersion and exercise and their effects on divers, high altitude climbers, astronauts and critically ill patients. It also conducts physiological studies in animal and cell models of disease as well as the role of oxygen and the other physiological gases on various biochemical and molecular pathways involved in pathogenesis.
Research in the Molecular Neurobiology Laboratory focuses on new strategies for organ protection by boosting highly conserved signaling pathways that nature has designed to protect cells from various forms of stress-induced damage. Small ubiquitin-like modifier (SUMO1-3) conjugation is an archetypical signaling pathway that is known to protect cells from various kinds of stress. Our data support the notion that targeting SUMO conjugation is a promising new strategy for protecting organs in the clinical setting. Our long-term goal is to improve outcomes in patients who suffer a stroke or other forms of brain ischemic injury.
The Multidisciplinary Neuroprotection Laboratory is dedicated to examining the pathophysiology of acute brain and spinal cord injury with particular reference to disease states managed in the perioperative or neurointensive care environments. Rodent recovery models of cerebral ischemia, traumatic brain injury, cardiopulmonary bypass, subarachnoid hemorrhage, spinal cord ischemia, and perinatal hypoxia have been established with requisite control of relevant physiologic variables. Experimental protocols examine the response of brain to these insults and seek to define appropriate therapeutic interventions.
The focus of the Molecular Pharmacology Laboratory is to understand the role of G protein-coupled receptors in human diseases. Our current focus is to examine the role of the Neurokinin-1/substance P receptor and its interactions with receptor tyrosine kinases in glioblastoma multiforme (GBM). The goal of these translational studies is to develop an effective therapy to halt the growth of GBM. An ongoing side project, which is being conducted in collaboration with several clinicians, is to understand the molecular basis of postoperative delirium.
The Nerve Injury and Pain Mechanism Laboratory is currently studying the biological mechanisms underlying the human response to nerve injury and surgery, in particular, the way injury induced neuroplasticity and inflammation often combine to cause chronic pain after surgery or trauma. We are using a systems biology approach to understand the molecular mechanisms of inflammation, focusing on nerve injury, chronic post-surgical pain, and the maladaptive processes involved in the transition from acute to chronic pain. We utilize reverse translational methodology, identifying pathways and targets of interest in human case-control studies, and subsequently validating those findings with animal models of nerve injury. This process focuses our research and improves our ability to discern clinically meaningful targets and future potential therapies.
Each year, millions of individuals undergo surgery for medically necessary conditions and are at risk for developing postoperative neurocognitive disorders. After a routine operation, such as orthopedic surgery, many patients experience acute cognitive deficits (delirium) that in some cases may evolve into long-term cognitive impairments, also known as postoperative cognitive dysfunction (POCD), and even permanent dementia.
The Neuroinflammation and Cognitive Outcomes Laboratory studies the mechanisms underlying postoperative neurocognitive disorders with a strong focus on neuroinflammation, innate immunity and behavior. Using an integrated interdisciplinary and translational approach, we are addressing the biological complexity of this disease using clinically relevant models combined with molecular, genetic, physiological and imaging techniques. Our aims are to define the underlying mechanisms leading to memory deficits after surgery and to develop safe strategies to resolve neuroinflammation in the perioperative setting.
Chronic pain is known as a health epidemic in the United States. It affects 100 million Americans with an annual cost of more than $600 billion nationwide. Unfortunately, the current treatments for chronic pain are inadequate. The main goal of the Pain Signaling and Plasticity Laboratory is to identify novel molecular and cellular mechanisms underlying the genesis of chronic pain, such as neuropathic pain after nerve trauma and chemotherapy and inflammatory pain after arthritis.
The lack of effective treatments to reduce the consequences of myocardial ischemia-reperfusion injury and the increased reliance on percutaneous and surgical treatments for coronary and valvular disease or end-stage heart failure make it critically important to identify new targets and strategies for cardioprotection.
The Systems Modeling of Perioperative Cardiovascular Injury and Adaptation Laboratory combines comparative biology approaches in multiple organisms with translational functional genomics to study the mechanisms underlying perioperative myocardial injury, with a particular emphasis on endogenous cardioprotective responses involving attenuation of nuclear factor-kappa B regulated inflammatory signaling and changes in myocardial fuel utilization.
Pain is a multidimensional sensory and emotional experience that is important for our survival. Acute pain occurs in response to environmental stimuli and warns us of potential or actual tissue damage. In the event of actual tissue damage, pain serves to promote wound healing and repair. However, in some cases the pain outlasts the stimulus and becomes chronic. Once pain becomes chronic, it is no longer beneficial and, instead, becomes a disorder in and of itself.
Although our understanding of pain neurobiology has grown over the last several years, few new therapeutics have been developed. Thus, it is imperative that further research be conducted to better understand chronic pain; its causes, effects, and treatments.
The three main objectives of The Nackley Lab include:
- To determine the factors that put some people, but not others, at risk for maladaptive chronic pain conditions
- To elucidate the mechanism(s) whereby genetic, biological, and environmental factors drive chronic pain
- To improve pharmacologic management of pain