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The nonopioid actions of spinal dynorphin may promote aspects of abnormal pain after nerve injury. Mechanistic similarities have been suggested between opioid tolerance and neuropathic pain. Here, the hypothesis that spinal dynorphin might mediate effects of sustained spinal opioids was explored. Possible abnormal pain and spinal antinociceptive tolerance(More)
Peripheral nerve injury produces signs of neuropathic pain including tactile allodynia and thermal hyperalgesia, sensory modalities which may be associated with different neuronal pathways. Studies of spinally-transected, nerve-injured rats have led to suggestions that thermal hyperalgesia may be mediated predominately through local spinal circuitry whereas(More)
Spinal nerve ligation produces signs of neuropathic pain in rats. Different neuronal pathways may underlie the abnormal sensory responses to thermal and tactile stimuli. Here, the possibility that local circuitry in the spinal cord and/or spinal-supraspinal loops might be involved in tactile allodynia and thermal hyperalgesia of the hindpaws was(More)
The activation of a complement system can aggravate the secondary injury after spinal cord injury (SCI). However, it was reported recently that the activation of a complement could have both a secondary injury and a neuroprotective effect, in which C5a is the most important factor, but there is no direct evidence for this dual effect of C5a after SCI. In(More)
STAR's measurements of directed flow (v1) around midrapidity for π±, K±, KS0, p, and p[over ¯] in Au+Au collisions at √[sNN]=200  GeV are presented. A negative v1(y) slope is observed for most of produced particles (π±, K±, KS0, and p[over ¯]). In 5%-30% central collisions, a sizable difference is present between the v1(y) slope of protons and antiprotons,(More)
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