S
Samuel S. Duffy
Researcher at University of New South Wales
Publications - 15
Citations - 719
Samuel S. Duffy is an academic researcher from University of New South Wales. The author has contributed to research in topics: Neuropathic pain & Multiple sclerosis. The author has an hindex of 11, co-authored 14 publications receiving 532 citations.
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Journal ArticleDOI
Characterisation of Immune and Neuroinflammatory Changes Associated with Chemotherapy-Induced Peripheral Neuropathy.
Preet G.S. Makker,Samuel S. Duffy,Justin G. Lees,Chamini J. Perera,Ryan S. Tonkin,Oleg Butovsky,Susanna B. Park,David Goldstein,Gila Moalem-Taylor +8 more
TL;DR: It is suggested that PTX and OXA cause distinct pathological changes in the periphery and nervous system, which may contribute to chemotherapy-induced neuropathic pain.
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The Contribution of Immune and Glial Cell Types in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis
TL;DR: Evidence of T and B lymphocyte, natural killer cell, macrophage/microglial, astrocytic, and oligodendroglial involvement in both EAE and MS and the intercommunication and influence of each cell subset in the inflammatory process are summarized.
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Attenuation of mechanical pain hypersensitivity by treatment with Peptide5, a connexin-43 mimetic peptide, involves inhibition of NLRP3 inflammasome in nerve-injured mice.
Ryan S. Tonkin,Callum Bowles,Chamini J. Perera,Brooke A Keating,Preet G.S. Makker,Samuel S. Duffy,Justin G. Lees,Collin Tran,Anthony S. Don,Thomas Fath,Lu Liu,Simon J. O'Carroll,Louise F.B. Nicholson,Colin R. Green,Catherine A. Gorrie,Gila Moalem-Taylor +15 more
TL;DR: It is demonstrated that blocking Cx43 hemichannels with Peptide5 after nerve injury attenuates mechanical pain hypersensitivity by specifically targeting the NLRP3 inflammasome in the spinal cord.
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The role of regulatory T cells in nervous system pathologies.
TL;DR: Emerging evidence for the dichotomous role of Treg cells in various neurological pathologies including multiple sclerosis, Guillain‐Barré syndrome, neuropathic pain, traumatic central nervous system injury, stroke, and neurodegenerative diseases such as amyotrophic lateral sclerosis, Alzheimer's disease, and Parkinson's disease is discussed.
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Depletion of Foxp3+ regulatory T cells increases severity of mechanical allodynia and significantly alters systemic cytokine levels following peripheral nerve injury
TL;DR: The results suggest that depletion of Foxp3+ Treg cells promote nerve injury-induced pain hypersensitivity, partially by inducing altered systemic concentrations of cytokines, which may act to regulate neuropathic pain.