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    Effects of a novel tripeptide on neurological outcomes after spinal cord injury.
    Neuroreport 2006 Nov;17(17):1793-6
    Spinal Cord Injury Team, BioTherapeutics Research Group, Robarts Research Institute, London, Ontario, Canada.
    A biologically active tripeptide [phenylalanine glutamate glycine (feG)] derived from the submandibular gland has anti-inflammatory actions. We have shown that intravenous treatment with feG after spinal cord injury decreases the intraspinal infiltration of leukocytes and associated oxidative damage within 72 h after injury. The present study assessed effects of this treatment on chronic neurological outcomes after clip-compression spinal cord injury at the 12th thoracic segment. Locomotor scores of feG-treated rats were significantly higher than those of controls at 7 weeks after spinal cord injury. Treated rats had significantly less hind paw mechanical allodynia than controls at this time. In conclusion, the anti-inflammatory and anti-oxidative actions of feG treatment correlate with improved neurological outcomes after spinal cord injury.

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    The tripeptide phenylalanine-(D) glutamate-(D) glycine modulates leukocyte infiltration and oxidative damage in rat injured spinal cord.
    Neuroscience 2006 Jul 3;140(3):1011-22. Epub 2006 Apr 3.
    Spinal Cord Injury Team, Laboratory of Spinal Cord Injury, BioTherapeutics Research Group, Robarts Research Institute, 100 Perth Drive, London, Ontario, Canada N6A 5K8.
    The tripeptide, phenylalanine-glutamate-glycine (FEG) and its d-isomeric form phenylalanine-(D) glutamate-(D) glycine (feG), derived from submandibular gland peptide-T, significantly reduce the allergic inflammatory response and leukocyte trafficking and neutrophil migration into intestine, heart and lungs. Due to these actions, we hypothesized that feG would attenuate the early inflammatory response to spinal cord injury, reduce free radical production and improve neurological outcomes, like other leukocyte-limiting strategies we have used previously. We tested this using a clip compression model of spinal cord injury in rats. Read More
    An integrin inhibiting molecule decreases oxidative damage and improves neurological function after spinal cord injury.
    Exp Neurol 2008 Dec 26;214(2):160-7. Epub 2008 Sep 26.
    Spinal Cord Injury Laboratory, BioTherapeutics Research Group, Robarts Research Institute, Schulich School of Medicine and Dentistry, The University of Western Ontario, PO Box 5015, 100 Perth Drive, London, Ontario Canada.
    Our previous studies have shown that treatment with an alpha4beta1 integrin blocking antibody after spinal cord injury (SCI) in rats decreases intraspinal inflammation and oxidative damage, improving neurological function. Here, we studied effects of a high affinity small molecule alpha4beta1 inhibitor, BIO5192. First, rats were treated intravenously with BIO5192 (10 mg/kg) or with vehicle (controls) to assess effects of integrin blockade for 24 h or 72 h after thoracic clip-compression SCI. Read More
    Transient blockade of the CD11d/CD18 integrin reduces secondary damage after spinal cord injury, improving sensory, autonomic, and motor function.
    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.
    The early inflammatory response to spinal cord injury (SCI) causes significant secondary damage. Strategies that nonselectively suppress inflammation have not improved outcomes after SCI, perhaps because inflammation has both adverse and beneficial effects after SCI. We have shown that the selective, time-limited action of a monoclonal antibody (mAb) to the CD11d subunit of the CD11d/CD18 integrin, delivered intravenously during the first 48 hr after SCI in rats, markedly decreases the infiltration of neutrophils and delays the entry of hematogenous monocyte-macrophages into the injured cord. Read More
    Alpha4beta1 integrin blockade after spinal cord injury decreases damage and improves neurological function.
    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