Francis Beaudry

This study compares the structural features of human and C. elegans alpha2delta subunits to assess gabapentinoid binding site conservation using docking and molecular dynamics simulations.

This study uses C. elegans to analyze the pharmacokinetic and pharmacodynamic relationships of gabapentinoids, showing dose- and time-dependent effects and a saturable pharmacodynamic ceiling.

This study shows that translational control in spinal cord neurons, particularly in inhibitory and PV+ interneurons, significantly influences gene expression and pain hypersensitivity during the chronic phase of neuropathic pain.

This study investigates the antinociceptive effects of four Cannabis sativa terpenes in C. elegans, showing their modulation of nociceptive responses and molecular pathways via TRPV-like and cannabinoid-like receptors.

This study investigates the antinociceptive effects of CBV and THCV in C. elegans, showing dose-dependent effects and involvement of vanilloid and cannabinoid pathways.

This study shows that fatty acid metabolism affects thermal nociception in C. elegans by linking PUFA biosynthesis to heat avoidance behavior.

The paper investigates how the deletion of the Tac1 gene affects kinase phosphorylation in spinal cord tissue, revealing altered signaling pathways linked to pain modulation and inflammatory responses.

This study identifies a systemic inflammatory proteomic profile in nerve-injured mice that contributes to neuropathic pain development.

The paper shows FSH activates JAK3 in bovine granulosa cells, increasing phosphorylation of STAT3 and other proteins, and modulating steroidogenesis and proliferation.

This study shows that RTX reduces nocifensive response in C. elegans to noxious heat and identifies Wnt signaling as a pathway involved.

This study shows capsaicin and its analogues reduce nocifensive response in C. elegans to noxious heat, with effects reversing after 6 hours.

This study shows that impaired EAT-4 vesicular glutamate transporters in C. elegans lead to defective thermal avoidance behavior, highlighting the role of glutamate signaling in nocifensive responses to noxious heat.