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Josephine Lai

Researcher at University of Arizona

Publications -  182
Citations -  14528

Josephine Lai is an academic researcher from University of Arizona. The author has contributed to research in topics: Receptor & Opioid. The author has an hindex of 60, co-authored 182 publications receiving 13914 citations.

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Potent and nontoxic antisense oligonucleotides containing locked nucleic acids

TL;DR: It is demonstrated here that a high-affinity DNA analog, locked nucleic acid (LNA), confers several desired properties to antisense agents, and LNA/DNA copolymers exhibited potent antisense activity on assay systems as disparate as a G-protein-coupled receptor in living rat brain and an Escherichia coli reporter gene.
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CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids.

TL;DR: Test the hypothesis that CB(2) receptor activation stimulates release from keratinocytes of the endogenous opioid beta-endorphin, which then acts at local neuronal mu-opioid receptors to inhibit nociception and indicates anatomical specificity of opioid effects.
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Unmasking the tonic-aversive state in neuropathic pain.

TL;DR: Conditioned place preference is used to concomitantly determine the presence of tonic pain in rats and the efficacy of agents that relieve it and provides a new approach for investigating tonicPain in animals and for evaluating the analgesic effects of drugs.
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Activation of CB2 cannabinoid receptors by AM1241 inhibits experimental neuropathic pain: Pain inhibition by receptors not present in the CNS

TL;DR: AM1241 dose-dependently reversed tactile and thermal hypersensitivity produced by ligation of the L5 and L6 spinal nerves in rats, demonstrating a mechanism leading to the inhibition of pain, one that targets receptors localized exclusively outside the CNS.
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Inhibition of neuropathic pain by decreased expression of the tetrodotoxin-resistant sodium channel, NaV1.8.

TL;DR: It is shown that intrathecal administration of specific antisense oligodeoxynucleotides (ODN) to the peripheral tetrodotoxin (TTX)‐resistant sodium channel, NaV1.8, resulted in a time‐dependent uptake of the ODN by dorsal root ganglion (DRG) neurons, and a selective ‘knock‐down’ of the expression of NaV 1.8 which reversed neuropathic pain induced by spinal nerve injury.