J Neurosci 2004 Apr;24(16):4043-51
Spinal Cord Injury Team, BioTherapeutics Research Group, Robarts Research Institute, University of Western Ontario, London, Ontario N6A 5K8, Canada.
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Exp Neurol 2008 Dec 1;214(2):147-59. Epub 2008 May 1.
Spinal Cord Injury Laboratory, BioTherapeutics Research Group, Robarts Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5K8.
The extent of disability caused by spinal cord injury (SCI) relates to secondary tissue destruction arising partly from an intraspinal influx of neutrophils and monocyte/macrophages after the initial injury. The integrin alpha4beta1, expressed by these leukocytes, is a key to their activation and migration into/within tissue. Therefore, blocking this integrin's functions may afford significant neuroprotection. Read More
Exp Neurol 2005 Aug;194(2):541-9
Spinal Cord Injury Team, Laboratory of Spinal Cord Injury, BioTherapeutics Research Group, Robarts Research Institute and Graduate Program in Neuroscience, University of Western Ontario, 100 Perth Drive, London, Ontario, Canada N6A 5K8.
Autonomic dysreflexia is a condition of episodic hypertension that develops after spinal cord injury (SCI). We previously showed that a two-day anti-inflammatory treatment with an anti-CD11d integrin monoclonal antibody (mAb), soon after SCI in rats, reduced the magnitude of dysreflexia for at least 6 weeks. Effects of methylprednisolone (MP), a commonly used neuroprotective treatment for SCI, on dysreflexia have never been examined. Read More
J Neurosci 2005 Jan;25(3):637-47
BioTherapeutics Research Group, Robarts Research Institute, The University of Western Ontario, London, Ontario, N6A 5K8, Canada.
Spinal serotonergic pathways provide inhibitory and excitatory modulation of sensory, autonomic, and motor processing. After spinal cord injury (SCI), the acute inflammatory response is one process that damages descending pathways. Increases in serotonergic fiber density in spinal segments rostral and decreases caudal to the lesion have been observed previously and may contribute to neuropathic pain and motor dysfunction associated with SCI. Read More
J Neurochem 2004 Mar;88(6):1335-44
Spinal Cord Injury Team, BioTherapeutics Research Group, Robarts Research Institute, London, Ontario, Canada.
We investigated mechanisms by which a monoclonal antibody (mAb) against the CD11d subunit of the leukocyte integrin CD11d/CD18 improves neurological recovery after spinal cord injury (SCI) in the rat. The effects of an anti-CD11d mAb treatment were assessed on ED-1 expression (estimating macrophage infiltration), myeloperoxidase activity (MPO, approximating neutrophil infiltration), lipid peroxidation, inducible nitric oxide synthase (iNOS) and nitrotyrosine (indicating protein nitration) expression in the spinal cord lesion after severe clip-compression injury. Protein expression was evaluated by western blotting and immunocytochemistry. Read More