Harmon JB, Sanders AE, Wilder RS, Essick GK, Slade GD, Hartung JE, Nackley AG. Circulating Omentin-1 and Chronic Painful Temporomandibular Disorders. J Oral Facial Pain Headache. 2016 Summer;30(3):203-209.
Ciszek BP, O’Buckley SC, Nackley AG. Persistent Catechol-O-methyltransferase-dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors. Anesthesiology. 2016 May;124(5):1122-35.
Oladosua FA, Ciszek BP, O’Buckley SC, Nackley AG. Novel Intrathecal and Subcutaneous Catheter Delivery Systems in the Mouse. Journal of Neuroscience Methods. 2016 Mar 11. pii: S0165-0270(16)30012-7. [Epub ahead of print]
Nackley A. Chronic Pain: Translating Discoveries Into Treatments. International Innovation. 2015 June;185:56-58.
2017 APS Young Investigator Travel Support Program awarded to Dr. Xin Zhang
Dr. Zhang will travel to, and present a poster at, the 36th Annual Scientific Meeting of the American Pain Society, held May 17-20, 2017 in Pittsburgh, Pennsylvania. APS gratefully acknowledges the National Center for Complementary and Integrative Health (NCCIH) for support of the Young Investigator Travel Award program.
Duke 2017 Summer Neuroscience Program Fellowship awarded to Katie Kanter
Title: Effects of MOR-1K Genetic Variation on Cellular Activity
Summary: Opioid induced hyperalgesia manifests as increased pain sensitivity due to acute or chronic opioid administration. A truncated variant in the mu opioid receptor, MOR-1K, has been linked to pain in human genetic studies, and shown to produce cellular excitation, resulting in hyperalgesia rather than analgesia.The Nackley Lab has identified a candidate single nucleotide polymorphism (SNP) within the enhancer box regulatory motif on MOR-1K exon 13 in CXB7/ByJ mice, that is predicted to contribute to the increased pain sensitivity observed in this variant compared to 129S6 mice. The proposed work will continue a previously unpublished study by the Nackley lab, to elucidate alterations to MOR-1K receptor function related to this SNP using a cAMP assay, and ultimately examine changes to transcriptional regulation via a luciferase assay.
NIH/NIDCR Grant # R56DE025296-01 awarded to Dr. Andrea Nackley
Title: Proteins, MicroRNAs and Genes Associated with TMD and Overlapping Conditions
Awarded Date: September 21, 2016
Summary: The Institute of Medicine found that chronic pain affects 100 million Americans, causing extensive economic, social, and personal costs. For some the pain remains localized, while for others the pain spreads to affect multiple anatomic sites, suggesting a common underlying cause. In response to PA-14-244, we plan to use stored biospecimens and existing data from a clinical study of 1,460 adults to determine biological (proteins, microRNAs, and gene polymorphisms), psychosocial (stress, depression, anxiety), and clinical (general health and environmental exposures) factors that contribute to localized and overlapping pain conditions. Further, we will use bioinformatics methods to understand how these factors interact to influence pain, with the long-term goal to identify biomarkers for the diagnosis and treatment of chronic overlapping pain conditions.
Brittney Ciszek PhD, is the first-place recipient of the 24th Annual Duke Anesthesiology Academic Evening’s Excellence in the Pre-Doctoral Non-Medical Student category.
Bomi Oladosu has been selected to receive the GPSF Excellence in Mentoring Award 2016. The award will be presented at the 18th Annual Graduate School Student Recognition Ceremony, scheduled for April 14 at the George Watts Hill Alumni Center, University of North Carolina at Chapel Hill.
F31 from NIAMS/NIH awarded to Jane Hartung
Title: The Role of TNF-alpha and MAP Kinases in the Maintenance of COMT-Dependent Pain
Date: 09/01/2015 – 08/31/2017
Summary: This proposal utilizes a unique animal model that mimics the genetics and physiology of chronic musculoskeletal pain conditions along with behavioral pharmacologic, immunocytochemical, and live animal imaging techniques to test the hypothesis that tumor necrosis factor alpha (TNFα) and mitogen-activated protein kinases (MAPKs) maintain COMT-dependent pain at cellular and behavioral levels.