FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1139140741> ?p ?o ?g. }

• W1139140741 abstract "Chronic pain affects billions and billions of people worldwide and its underlying mechanisms responsible are vast and poorly understood. Both neural and immune mechanisms play a role in the development and maintenance of chronic pain. Toll-like receptors (TLRs) are a family of receptors that play a key role in the innate immune system, many of which are associated with foreign bodies or genomic material derived from pathogens. Additionally, TLRs are also activated by endogenous cell components secondary to cell death, endocytosis, and inflammatory tissue damage. Although TLRs are widely known to play a role in the response to infectious processes, current work indicates the presence of endogenous TLRs in the nervous system, particularly on non-neuronal, glial cells. These non-neuronal, glial cells are mechanistically involved in regulating local system excitability secondary to high intensity afferent input and nerve injury. This organization suggests that TLRs may play a role in mediating spinal sensitization initiated by peripheral stimulation. I aim to characterize the role of spinal TLRs and define their contribution to the spinal processing of nociceptive information. Organizing hypothesis : Following nerve injury, the activation of TLRs contributes to spinal sensitization due to their direct activation of non- neuronal cells and the resulting release of central pain mediators. Additionally, TLRs and their signaling intermediaries, or adaptor proteins, determine the recovery pathway after initial insult. To investigate the above hypotheses, I will utilize both in vitro and in vivo models and will undertake experiments to address three primary aims : (1) Determine which TLRs present on primary astrocyte and microglial cells initiate glial activation, as assessed by cytokine and interferon release; (2) Determine the role of spinal TLRs in the facilitated pain state and the contribution of specific TLR adaptor proteins following acute pain; (3) Establish the role of TLR activation in the associated hyperalgesia produced by peripheral nerve injury, and assess glial activation and contribution of adaptor proteins to this hyperalgesic state. Taken together these studies will define the role of the several TLRs in regulating dorsal horn excitability leading to behaviorally defined changes in pain processing" @default.
• W1139140741 created "2016-06-24" @default.
• W1139140741 creator A5090959575 @default.
• W1139140741 date "2013-01-01" @default.
• W1139140741 modified "2023-09-27" @default.
• W1139140741 title "Spinal toll-like receptors and nociceptive processing" @default.
• W1139140741 hasPublicationYear "2013" @default.
• W1139140741 type Work @default.
• W1139140741 sameAs 1139140741 @default.
• W1139140741 citedByCount "0" @default.
• W1139140741 crossrefType "journal-article" @default.
• W1139140741 hasAuthorship W1139140741A5090959575 @default.
• W1139140741 hasConcept C136449434 @default.
• W1139140741 hasConcept C15490471 @default.
• W1139140741 hasConcept C169760540 @default.
• W1139140741 hasConcept C170493617 @default.
• W1139140741 hasConcept C172659308 @default.
• W1139140741 hasConcept C203014093 @default.
• W1139140741 hasConcept C2776709828 @default.
• W1139140741 hasConcept C55493867 @default.
• W1139140741 hasConcept C86803240 @default.
• W1139140741 hasConcept C8891405 @default.
• W1139140741 hasConcept C95444343 @default.
• W1139140741 hasConceptScore W1139140741C136449434 @default.
• W1139140741 hasConceptScore W1139140741C15490471 @default.
• W1139140741 hasConceptScore W1139140741C169760540 @default.
• W1139140741 hasConceptScore W1139140741C170493617 @default.
• W1139140741 hasConceptScore W1139140741C172659308 @default.
• W1139140741 hasConceptScore W1139140741C203014093 @default.
• W1139140741 hasConceptScore W1139140741C2776709828 @default.
• W1139140741 hasConceptScore W1139140741C55493867 @default.
• W1139140741 hasConceptScore W1139140741C86803240 @default.
• W1139140741 hasConceptScore W1139140741C8891405 @default.
• W1139140741 hasConceptScore W1139140741C95444343 @default.
• W1139140741 hasLocation W11391407411 @default.
• W1139140741 hasOpenAccess W1139140741 @default.
• W1139140741 hasPrimaryLocation W11391407411 @default.
• W1139140741 hasRelatedWork W1767777404 @default.
• W1139140741 hasRelatedWork W2004622194 @default.
• W1139140741 hasRelatedWork W2012628595 @default.
• W1139140741 hasRelatedWork W2013100814 @default.
• W1139140741 hasRelatedWork W2034088074 @default.
• W1139140741 hasRelatedWork W2040892689 @default.
• W1139140741 hasRelatedWork W2045716655 @default.
• W1139140741 hasRelatedWork W2067505623 @default.
• W1139140741 hasRelatedWork W2121347099 @default.
• W1139140741 hasRelatedWork W2187289551 @default.
• W1139140741 hasRelatedWork W2222298767 @default.
• W1139140741 hasRelatedWork W2318283819 @default.
• W1139140741 hasRelatedWork W2318624728 @default.
• W1139140741 hasRelatedWork W2354878433 @default.
• W1139140741 hasRelatedWork W2358506615 @default.
• W1139140741 hasRelatedWork W2755801421 @default.
• W1139140741 hasRelatedWork W2995976092 @default.
• W1139140741 hasRelatedWork W3092225052 @default.
• W1139140741 hasRelatedWork W3134131019 @default.
• W1139140741 hasRelatedWork W3151507532 @default.
• W1139140741 isParatext "false" @default.
• W1139140741 isRetracted "false" @default.
• W1139140741 magId "1139140741" @default.
• W1139140741 workType "article" @default.