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quisqualic acid/entzündung
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12 Ergebnisse
Neuronal degeneration and spinal cavitation following intraspinal injections of quisqualic acid in the rat.
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Microinjections of quisqualic acid were made in the spinal cord to evaluate the excitotoxic effects of this excitatory amino acid agonist on spinal neurons in the rat. Animals were divided into four groups based on post injection survival times of 7-49 days. Injections ranging from 0.3 to 2.0 microL
The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo.
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Brain inflammatory processes underlie the pathogenesis of Alzheimer's disease, and non-steroidal anti-inflammatory drugs have a protective effect in the disease. The aim of this work was to study in vivo whether attenuation of brain inflammatory response to excitotoxic insult by the selective
Brain inflammatory reaction in an animal model of neuronal degeneration and its modulation by an anti-inflammatory drug: implication in Alzheimer's disease.
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Brain inflammatory processes underlie the pathogenesis of Alzheimer's disease, and nonsteroidal anti-inflammatory drugs have a protective effect in the disease. The aim of this study was to characterize in vivo in the rat brain the inflammatory reaction in response to excitotoxic insult and to
NO-flurbiprofen attenuates excitotoxin-induced brain inflammation, and releases nitric oxide in the brain.
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Brain inflammation underlies the pathogenesis of Alzheimer's disease (AD) and nonsteroidal anti-inflammatory drug therapy may delay the onset of AD. We investigated, in vivo, the effects of NO-flurbiprofen on brain inflammation in rats injected with quisqualic acid into the nucleus basalis and on
Effects of interleukin-10 (IL-10) on pain behavior and gene expression following excitotoxic spinal cord injury in the rat.
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Intraspinal injection of quisqualic acid (QUIS) produces excitotoxic injury with pathophysiological characteristics similar to those associated with ischemic and traumatic spinal cord injury (SCI). Responses to QUIS-induced injury include an inflammatory component, as well as the development of
Neuroprotective effects of interleukin-10 following excitotoxic spinal cord injury.
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Intraspinal injection of quisqualic acid (QUIS) produces excitotoxic injury with pathological characteristics similar to those associated with ischemic and traumatic spinal cord injury (SCI). Inflammatory responses appear to be a major component of the secondary neuronal injury initiated by SCI and
Neuroprotective effects of nicotinamide after experimental spinal cord injury.
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OBJECTIVE
To investigate the ability of nicotinamide to protect against secondary damage in spinal cord tissue after an experimental injury. Trauma to the spinal cord induces a cascade of cellular events that lead to progressive tissue injury over time. Nicotinamide has been shown to affect many
The effects of endogenous interleukin-10 on gray matter damage and the development of pain behaviors following excitotoxic spinal cord injury in the mouse.
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Interleukin-10 (IL-10) has been utilized as a neuroprotective agent in experimental models of spinal cord injury because of its potent anti-inflammatory properties. Previous studies have delivered a single dose (5 microg) of IL-10 following experimental spinal cord injury in the rat, and
Inhibitory effect of new quinolones on GABA(A) receptor-mediated response and its potentiation with felbinac in Xenopus oocytes injected with mouse-brain mRNA: correlation with convulsive potency in vivo.
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Convulsions induced by the interaction of new quinolone antimicrobial agents (NQs) and nonsteroidal anti-inflammatory drugs (NSAIDs) were previously reported, and blockade of GABA(A) receptor by NQs and its potentiation with NSAIDs were considered as one of its possible mechanisms. However, useful
Spinal and supraspinal changes in tumor necrosis factor-alpha expression following excitotoxic spinal cord injury.
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The role of tumor necrosis factor-alpha (TNF-alpha) after spinal cord injury (SCI) is well characterized in the cord, but the impact of this inflammatory process on supraspinal levels is unknown. This study examines TNF-alpha mRNA and protein levels in the brains and spinal cords of mice after SCI.
Reaction of endogenous progenitor cells in a rat model of posttraumatic syringomyelia.
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OBJECTIVE
Endogenous stem cells theoretically could replace lost tissue and repair deficits caused by syringes. In this study the authors quantitatively examined 1) whether neural progenitor cells exist in an adult rat model of posttraumatic syringomyelia (PTS); 2) and if so, how long an active
Diffusion-weighted MR imaging in a rat model of syringomyelia after excitotoxic spinal cord injury.
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OBJECTIVE
Recent experimental data have shown that an increase of excitatory amino acids and the initiation of inflammatory responses within the injured spinal cord may play a role in post-traumatic syringomyelia. The purpose of this study was to determine whether diffusion-weighted MR imaging with
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