F
Flobert Y. Tanga
Researcher at Dartmouth College
Publications - 7
Citations - 2013
Flobert Y. Tanga is an academic researcher from Dartmouth College. The author has contributed to research in topics: Neuropathic pain & Proinflammatory cytokine. The author has an hindex of 6, co-authored 7 publications receiving 1908 citations.
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Inhibition of Microglial Activation Attenuates the Development but not Existing Hypersensitivity in a Rat Model of Neuropathy
TL;DR: It is demonstrated that inhibition of microglial activation attenuated the development of behavioral hypersensitivity in a rat model of neuropathic pain but had no effect on the treatment of existing mechanical allodynia and hyperalgesia.
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The CNS role of Toll-like receptor 4 in innate neuroimmunity and painful neuropathy
TL;DR: A critical role for CNS innate immunity by means of microglial Toll-like receptor 4 (TLR4) in the induction phase of behavioral hypersensitivity in a mouse and rat model of neuropathy is demonstrated for the first time.
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Neuroimmune Activation and Neuroinflammation in Chronic Pain and Opioid Tolerance/Hyperalgesia:
TL;DR: The challenge remains in the careful perturbation of injury/opioid-induced neuroimmune activation to down-regulate this process without inhibiting beneficial CNS autoimmunity that subserves neuronal protection following injury.
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Toll-like receptor 2 (TLR2) mediates astrocyte activation in response to the Gram-positive bacterium Staphylococcus aureus.
TL;DR: It is demonstrated that primary astrocytes are capable of recognizing the Gram‐positive bacterium Staphylococcus aureus and its cell wall product peptidoglycan and respond by producing numerous proinflammatory mediators and Toll‐like receptor 2 is essential for maximal proinflammatory cytokine and chemokine production.
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Differential spinal cord gene expression in rodent models of radicular and neuropathic pain.
Michael L. LaCroix-Fralish,Vivianne L. Tawfik,Flobert Y. Tanga,Kevin F. Spratt,Joyce A. DeLeo +4 more
TL;DR: These results suggest that diverging mechanisms lead to a common behavioral outcome in these pain models, and may implicate unique drug therapies for these types of chronic pain syndromes.