Robert R. Myers
University of California, San Diego
169 Papers
2.6K Citations
Robert R. Myers is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Sciatic nerve & Nerve injury. The author has an hindex of 58, co-authored 169 publications. Previous affiliations of Robert R. Myers include Indiana University – Purdue University Indianapolis & Fukushima Medical University.
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Papers
Involvement of Cytokines in Lipopolysaccharide-Induced Facilitation of CGRP Release from Capsaicin-Sensitive Nerves in the Trachea: Studies with Interleukin-1β and Tumor Necrosis Factor-α
TL;DR: The findings suggest that endotoxin treatment generated cytokines such as IL-1β and TNF-α that regulated the peripheral releasing function of primary sensory afferents by sensitizing the terminals and facilitating peptide release is prostanoid dependent.
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Relative neural toxicity of local anesthetics
TL;DR: Both nerve injury and edema increased with concentration of local anesthetics, but injury was frequently present in nerve fascicles with little or no edema, not consistent with the proposal that ester-linked agents are more likely than other local anesthetic agents to cause nerve injury.
104
Erythropoietin reduces Schwann cell TNF-α, Wallerian degeneration and pain-related behaviors after peripheral nerve injury
TL;DR: It is demonstrated that systemically administered recombinant human erythropoietin (rhEpo) facilitates recovery from chronic neuropathic pain associated with CCI in rats, and suggests a model in which rhEpo counteracts the effects of TNF‐α in CCI by blocking expression of T NF‐ α in Schwann cells.
103
•Journal Article
Quantitative histologic analysis of local anesthetic-induced injury to rat sciatic nerve.
TL;DR: Quantitative data on the specificity of the regional distribution of nerve injury and of Schwann cell effects are consistent with a direct cellular toxicity of the local anesthetics; however, these results do not preclude a role for toxicity mediated indirectly by changes in the endoneurial environment.
101
Inhibition of p38 MAP kinase activity enhances axonal regeneration.
Robert R. Myers,Yasufumi Sekiguchi,Shinichi Kikuchi,Brian W. Scott,Satya Medicherla,Andrew A. Protter,W. Marie Campana +6 more
TL;DR: It is shown that inhibition of p38 activity promotes axonal regeneration through interactions with SC signaling and TNF activity, and SD-169 significantly reduced TNF-mediated primary SC death in culture experiments.
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