Shad B. Smith

ORCID: 0000-0002-2056-225X
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About
Contact & Profiles
Research Areas
  • Pain Mechanisms and Treatments
  • Fibromyalgia and Chronic Fatigue Syndrome Research
  • Botulinum Toxin and Related Neurological Disorders
  • Temporomandibular Joint Disorders
  • Musculoskeletal pain and rehabilitation
  • Neuropeptides and Animal Physiology
  • Pain Management and Placebo Effect
  • Nutrition, Genetics, and Disease
  • Peripheral Nerve Disorders
  • Ion channel regulation and function
  • Peripheral Neuropathies and Disorders
  • HIV Research and Treatment
  • Genetic Associations and Epidemiology
  • Orthopedic Surgery and Rehabilitation
  • Genetic and phenotypic traits in livestock
  • Stress Responses and Cortisol
  • Pharmacological Effects of Natural Compounds
  • Neurobiology and Insect Physiology Research
  • Cancer Treatment and Pharmacology
  • Muscle activation and electromyography studies
  • Receptor Mechanisms and Signaling
  • Genetics and Physical Performance
  • Hereditary Neurological Disorders
  • Pain Management and Opioid Use
  • Heart Rate Variability and Autonomic Control

Duke University
2016-2024

Duke Medical Center
2017-2024

Duke University Hospital
2017-2022

Brigham and Women's Hospital
2022

University of North Carolina at Chapel Hill
2009-2017

PreClinOmics (United States)
2017

Baidu (China)
2016

Center for Pain and the Brain
2016

TMJ Association
2014

McGill University
2003-2011

Empathy is thought to be unique higher primates, possibly humans alone. We report the modulation of pain sensitivity in mice produced solely by exposure their cagemates, but not strangers, pain. Mice tested dyads and given an identical noxious stimulus displayed increased behaviors with statistically greater co-occurrence, effects dependent on visual observation. When familiar were stimuli different intensities, behavior was influenced neighbor's status bidirectionally. Finally, observation...

10.1126/science.1128322 article EN Science 2006-06-30

The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating severe episodic in paroxysmal extreme disorder and primary erythermalgia. This led us to investigate whether single nucleotide polymorphisms (SNPs) were associated with differing perception the general population. We first genotyped 27 SNPs 578 individuals radiographic diagnosis osteoarthritis score assessment. A significant association was found between SNP...

10.1073/pnas.0913181107 article EN Proceedings of the National Academy of Sciences 2010-03-08

Not all patients with nerve injury develop neuropathic pain. The extent of damage and age at the time are two few risk factors identified to date. In addition, preclinical studies show that pain variance is heritable. To define such further, we performed a large-scale gene profiling experiment which plotted global expression changes in rat dorsal root ganglion three peripheral models. This resulted discovery potassium channel alpha subunit KCNS1, involved neuronal excitability,...

10.1093/brain/awq195 article EN Brain 2010-08-19

It is generally believed that opioids relieve neuropathic pain less effectively than nociceptive and they have no effect on some of the key characteristics such as touch-evoked (allodynia). Tramadol an analgesic drug acting directly opioid receptors indirectly monoaminergic receptor systems. The aim this trial was to determine whether tramadol relieved painful polyneuropathy reduced allodynia. study design randomised, double-blind, placebo-controlled cross-over. After baseline observations,...

10.1016/s0304-3959(99)00079-2 article EN Pain 1999-10-01

Three common haplotypes in the gene encoding catechol-O-methyltransferase (COMT) have been associated with pain modulation and risk of developing chronic musculoskeletal pain, namely temporomandibular disorder (TMD). Haplotypes coding for higher enzymatic activity were correlated lower perception. Rodent studies showed that COMT inhibition increases sensitivity through beta2/3-adrenergic receptors. We hypothesized nonselective beta-adrenergic antagonist propranolol will reduce clinical...

10.1097/fpc.0b013e328337f9ab article EN Pharmacogenetics and Genomics 2010-03-18

For reasons unknown, temporomandibular disorder (TMD) can manifest as localized pain or in conjunction with widespread pain. We evaluated relationships between cytokines and TMD without palpation tenderness (TMD-WPT TMD+WPT, respectively) at protein, transcription factory activity, gene levels. Additionally, we the relationship intermediate phenotypes characteristic of WPT. In a case-control study 344 females, blood samples were analyzed for levels 22 activity 48 factors. Intermediate...

10.1016/j.pain.2011.09.005 article EN Pain 2011-10-17

In Brief The classification of most chronic pain disorders gives emphasis to anatomical location the distinguish one disorder from other (eg, back vs temporomandibular [TMD]) or define subtypes TMD myalgia arthralgia). However, criteria overlook etiology, potentially hampering treatment decisions. This study identified clusters individuals using a comprehensive array biopsychosocial measures. Data were collected case–control 1031 cases and 3247 TMD-free controls. Three subgroups supervised...

10.1097/j.pain.0000000000000518 article EN Pain 2016-03-01

Chronic pain is a highly prevalent and poorly managed human health problem. We used microarray-based expression genomics in 25 inbred mouse strains to identify dorsal root ganglion (DRG)-expressed genetic contributors mechanical allodynia, prominent symptom of chronic pain. identified levels Chrna6, which encodes the α6 subunit nicotinic acetylcholine receptor (nAChR), as associated with allodynia. confirmed importance α6* (α6-containing) nAChRs by analyzing both gain- loss-of-function...

10.1126/scitranslmed.3009986 article EN Science Translational Medicine 2015-05-13

The EGFR belongs to the well-studied ErbB family of receptor tyrosine kinases. is activated by numerous endogenous ligands that promote cellular growth, proliferation, and tissue regeneration. In present study, we have demonstrated a role for its natural ligand, epiregulin (EREG), in pain processing. We show inhibition with clinically available compounds strongly reduced nocifensive behavior mouse models inflammatory chronic pain. EREG-mediated activation enhanced nociception through...

10.1172/jci87406 article EN Journal of Clinical Investigation 2017-08-06

Heat sensitivity shows considerable functional variability in humans and laboratory animals, is fundamental to inflammatory possibly neuropathic pain. In the mouse, at least, much of this genetic because inbred strains differ robustly their behavioral noxious heat. These strain differences are shown here reflect differential responsiveness primary afferent thermal nociceptors heat stimuli. We further present convergent electrophysiological evidence that variable responses due...

10.1073/pnas.0503264102 article EN Proceedings of the National Academy of Sciences 2005-08-23

The aim of this study is to examine the difference in report bodily pain experienced by patients who develop temporomandibular disorders (TMD) and those do not TMD over a 3-year observation period.This prospective 266 females aged 18 34 years initially free pain. All completed Symptom Report Questionnaire (SRQ) at baseline yearly intervals, time they developed (if applicable). SRQ self-report instrument evaluating extent location earlier 6 months. Statistical analysis was carried out using...

10.1097/ajp.0b013e3181c507ef article EN Clinical Journal of Pain 2010-01-19

Abstract Objective Fibromyalgia (FM) represents a complex disorder that is characterized by widespread pain and tenderness frequently accompanied additional somatic cognitive/affective symptoms. Genetic risk factors are known to contribute the etiology of syndrome. The aim this study was examine >350 genes for association with FM, using large‐scale candidate gene approach. Methods group comprised 496 patients FM (cases) 348 individuals no chronic (controls). Genotyping performed dedicated...

10.1002/art.33338 article EN Arthritis & Rheumatism 2011-09-08

The effects of COMT genetic polymorphism on pain and analgesia are modality – selective gender dependent, in both mouse humanPlease approve Summary as edited. enzyme catechol-O-methyltransferase (COMT) metabolizes catecholamine neurotransmitters involved a number physiological functions, including perception. Both human genes possess functional polymorphisms contributing to interindividual variability phenotypes such sensitivity noxious stimuli, severity clinical pain, response treatment. In...

10.1016/j.pain.2013.04.028 article EN Pain 2013-04-18

Genetic interactions between catechol-O-methyltransferase val158met with estrogen receptor 1 and guanosine-5-triphosphate cyclohydrolase polymorphisms modulate downstream effects, including enzymatic activity, pain sensitivity, disease risk, psychological profile. Abnormalities in the activity of (COMT) contribute to chronic conditions, such as temporomandibular disorders (TMD). Thus, we sought determine effects COMT functionally related genes pathway (estrogen [ESR1], [GCH1],...

10.1016/j.pain.2014.09.009 article EN Pain 2014-09-16
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