According to the Institute of Medicine (IOM) report on Relieving Pain in America (June, 2011), chronic pain is a public health epidemic affecting more than 116 million Americans and costing more than $600 billion per year in healthcare expenses and lost work productivity. More Americans suffer from pain than those afflicted with heart disease, diabetes and cancer combined. Despite recent advances in treatment, most patients do not obtain adequate pain relief. Decades of pain research have produced few druggable targets, thus new approaches that take into account not just pain, but also comorbid pain conditions and individual differences (e.g., genetic and genomic variation) are needed. The conceptual basis for this core and center application acknowledges that nociception (neural processing of noxious stimulation) and pain (unpleasant emotional experience) are multifactorial and that co-morbidities, for example depression, anxiety, stress, and fear, and individual susceptibility (e.g., genetics and genomics) significantly influence these processes (Maixner et al., 2011). The University of Maryland Center for the Genomics of Pain (hereafter referred to as the """"""""Center"""""""") is dedicated to advancing the science of chronic pain research that incorporates the measurement of comorbid conditions and evaluation of genomics in basic, translational and clinical studies. To achieve our objectives, we will enhance our campus research infrastructure to increase the quantity and quality of interdisciplinary chronic pain studies that incorporate these measures. A number of faculty collaborate on cancer pain research in our current NINR P30 Center for Cancer Pain. This research program, recognized as a Developing Program, has now moved formally into the Greenebaum Cancer Center and is thriving. Subsequent to the release of the recent IOM report on chronic pain, we recognized the need to expand pain research on campus to more broadly focus on chronic pain conditions. After carefully considering the focus, we chose to expand in the area of genomics and also, address risk phenotypes (e.g., depression, fear, anxiety, stress). This will bring new collaborators with expertise in behavioral phenotyping and genomics into the pain research field. Center funding will enable us to formalize, enhance, and enact plans to sustain this new Center on campus. Our commitment to chronic pain research through Center activities will be facilitated through the following five Administrative Core (AC) Aims:
Aim 1. Provide oversight and coordination of administrative functions of the Center, including utilization of funds by the Cores and Pilot PIs, and ensure that funds are expended appropriately.
Aim 2. Optimize and enhance Core resource utilization at our campus and across the University of Maryland System (USM).
Aim 3. Establish, maintain and grow the Center website as a portal for chronic pain research on the University of Maryland Baltimore campus and as a mechanism for dissemination of Center activities to the broader pain, science and patient communities.
Aim 4. Plan for and actively pursue intramural, extramural and foundation funding to sustain and expand the Center research activities, during and beyond the P30 funding period.
Aim 5. Ensure the effectiveness of the Center to achieve its stated outcomes, including successful completion of pilot studies, creation of sustainable infrastructure for shared resources to facilitate interprofessional pain genomics research, and the dissemination of Center activities at the campus, regional, national and international levels.
These aims are relevant to the mission of the Center, and indeed, to building the capacity and infrastructure to support, grow, and sustain interdisciplinary pain research on the University of Maryland Baltimore campus and in the School of Nursing.
|Hertz, Daniel L; Owzar, Kouros; Lessans, Sherrie et al. (2016) Pharmacogenetic Discovery in CALGB (Alliance) 90401 and Mechanistic Validation of a VAC14 Polymorphism that Increases Risk of Docetaxel-Induced Neuropathy. Clin Cancer Res 22:4890-4900|
|Wu, Junfang; Zhao, Zaorui; Kumar, Alok et al. (2016) Endoplasmic Reticulum Stress and Disrupted Neurogenesis in the Brain Are Associated with Cognitive Impairment and Depressive-Like Behavior after Spinal Cord Injury. J Neurotrauma 33:1919-1935|
|Wu, Junfang; Zhao, Zaorui; Zhu, Xiya et al. (2016) Cell cycle inhibition limits development and maintenance of neuropathic pain following spinal cord injury. Pain 157:488-503|
|Starkweather, Angela R; Heineman, Amy; Storey, Shannon et al. (2016) Methods to measure peripheral and central sensitization using quantitative sensory testing: A focus on individuals with low back pain. Appl Nurs Res 29:237-41|
|Starkweather, Angela R; Ramesh, Divya; Lyon, Debra E et al. (2016) Acute Low Back Pain: Differential Somatosensory Function and Gene Expression Compared With Healthy No-Pain Controls. Clin J Pain 32:933-939|
|Redeker, Nancy S; Anderson, Ruth; Bakken, Suzanne et al. (2015) Advancing Symptom Science Through Use of Common Data Elements. J Nurs Scholarsh 47:379-88|
|Colagiuri, B; Schenk, L A; Kessler, M D et al. (2015) The placebo effect: From concepts to genes. Neuroscience 307:171-90|
|Lipinski, Marta M; Wu, Junfang; Faden, Alan I et al. (2015) Function and Mechanisms of Autophagy in Brain and Spinal Cord Trauma. Antioxid Redox Signal 23:565-77|
|Ellero-Simatos, Sandrine; Beitelshees, Amber L; Lewis, Joshua P et al. (2015) Oxylipid Profile of Low-Dose Aspirin Exposure: A Pharmacometabolomics Study. J Am Heart Assoc 4:e002203|
|Grimm, P Richard; Lazo-Fernandez, Yoskaly; Delpire, Eric et al. (2015) Integrated compensatory network is activated in the absence of NCC phosphorylation. J Clin Invest 125:2136-50|
Showing the most recent 10 out of 12 publications