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  1. Incidence and risk factors for pelvic pain following mesh implant surgery for the treatment of pelvic floor disorders
  2. Persistent Catechol-O-methyltransferase–dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors
  3. (374) Distinct mechanisms underlie the development and maintenance of COMT-dependent pain
  4. (363) Strain-specific polymorphisms and their correlation to MOR-1K receptor function
  5. (312) Peripherally located β2- and β3-adrenergic receptors contribute to the development of COMT-dependent pain in rats, but not the maintenance of pain in COMT-/- mice
  6. Circulating Omentin-1 and Chronic Painful Temporomandibular Disorders
  7. MicroRNA expression profiles differentiate chronic pain condition subtypes
  8. Nuclear factor-kappa B regulates pain and COMT expression in a rodent model of inflammation
  9. Alternative Splicing of G Protein–Coupled Receptors: Relevance to Pain Management
  10. Genetic Variants in Cyclooxygenase-2 Contribute to Post-treatment Pain among Endodontic Patients
  11. Catechol-O-methyltransferase inhibition alters pain and anxiety-related volitional behaviors through activation of β-adrenergic receptors in the rat
  12. Prevalence and Risk Factors for Pelvic Pain following Mesh Implant Surgery for the Treatment of Pelvic Organ Prolapse and Stress Urinary Incontinence
  13. 127. B2-and B3-adrenergic receptors drive the development of COMT-dependent pain by increasing release of NO and innate immune cytokines
  14. β2- and β3-adrenergic receptors drive COMT-dependent pain by increasing production of nitric oxide and cytokines
  15. Molecular correlates of localized versus co-occurring chronic pain conditions
  16. Multisystem Dysregulation in Painful Temporomandibular Disorders
  17. Excess Risk of Temporomandibular Disorder Associated With Cigarette Smoking in Young Adults
  18. Cytokine biomarkers and chronic pain: Association of genes, transcription, and circulating proteins with temporomandibular disorders and widespread palpation tenderness
  19. Cytokines associated with TMD case status and related intermediate phenotypes
  20. Assessing Potential Functionality of Catechol-O-methyltransferase (COMT) Polymorphisms Associated with Pain Sensitivity and Temporomandibular Joint Disorders
  21. A Novel alternatively spliced isoform of the mu-opioid receptor: functional antagonism
  22. Characterization of NF-kB-mediated inhibition of catechol-O-methyltransferase
  23. (169) Proinflammatory cytokine profiles associated with TMD case status and related intermediate phenotypes
  24. Genetic architecture of human pain perception
  25. Responses to Drs. Kim and Dionne regarding comments on Diatchenko, et al. Catechol-O-methyltransferase gene polymorphisms are associated with multiple pain-evoking stimuli. Pain 2006;125:216–24
  26. Catechol-O-methyltransferase inhibition increases pain sensitivity through activation of both β2- and β3-adrenergic receptors
  27. (649)
  28. (610)
  29. Catechol-O-methyltransferase gene polymorphisms are associated with multiple pain-evoking stimuli
  30. Idiopathic pain disorders – Pathways of vulnerability
  31. Perspectives on the Genetic Basis of Opioid-induced Hyperalgesia
  32. Neonatal Chronic Hind Paw Inflammation Alters Sensitization to Intradermal Capsaicin in Adult Rats: A Behavioral and Immunocytochemical Study
  33. Basal and carrageenan-induced pain behavior in Sprague–Dawley, Lewis and Fischer rats
  34. Genetic differences in basal and inflammatory pain behavior and in morphine’s analgesic effects in the rat
  35. Activation of Cannabinoid CB2 Receptors Suppresses C-Fiber Responses and Windup in Spinal Wide Dynamic Range Neurons in the Absence and Presence of Inflammation
  36. Selective activation of cannabinoid CB2 receptors suppresses spinal fos protein expression and pain behavior in a rat model of inflammation
  37. A peripheral cannabinoid mechanism suppresses spinal fos protein expression and pain behavior in a rat model of inflammation