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Ilona Obara

Researcher at Durham University

Publications -  12
Citations -  328

Ilona Obara is an academic researcher from Durham University. The author has contributed to research in topics: Neuropathic pain & Allodynia. The author has an hindex of 10, co-authored 12 publications receiving 301 citations. Previous affiliations of Ilona Obara include University of Castilla–La Mancha & Polish Academy of Sciences.

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Journal Article

Comparison of gene expression profiles in neuropathic and inflammatory pain.

TL;DR: The data point at the importance of immune response- and microglia activation-related genes in the development of chronic neuropathic pain, and suggest that expression of CGRP gene in the dorsal horn of the spinal cord could be involved in persistence of its symptoms.
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The Effects of Local Pentoxifylline and Propentofylline Treatment on Formalin-Induced Pain and Tumor Necrosis Factor- Messenger RNA Levels in the Inflamed Tissue of the Rat Paw

TL;DR: This study demonstrates and provides biochemical evidence that preemptive inhibition of proinflammatory cytokine synthesis by the use of PTF and PPTF, phosphodiesterase, and glial activation inhibitors is useful in antagonizing hyperalgesia in formalin-induced pain.
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Nonparalytic botulinum molecules for the control of pain

TL;DR: Results suggest that BiTox should be considered for treatment of pain conditions in which A-nociceptors are thought to play a significant role, and imply that although local release of neuromodulators from C-fibers was inhibited byBiTox injection, C- nociceptive signaling function was not impaired.
Journal Article

Efficacy of tramadol in combination with doxepin or venlafaxine in inhibition of nociceptive process in the rat model of neuropathic pain: an isobolographic analysis.

TL;DR: Isobolographic analysis for equivalent doses of drugs was applied to examine the nature of interaction between tramadol and doxepin or venlafaxine in a neuropathic pain model in rats, demonstrating synergistic action in reducing thermal hyperalgesia and additiveaction in reducing mechanical allodynia.