Publications by authors named "E J Redford"

Purpose: People with dementia (PWD) are one of the fastest-growing clinical populations for speech-language pathologists. Self-reported quality of life (QoL) assessments are critical patient-reported outcome measures that align with person-centered care principles. However, proxy-reporting is most often used due to assumptions that PWD cannot provide reliable self-report.

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Following the discovery of RPR200765, a series of pyrimidine analogues have been prepared as backups. Amongst them, RPR203494 was identified with a better in vitro profile than RPR200765A.

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RPR132331, a 2-(2-dioxanyl)imidazole, was identified as an inhibitor of tumour necrosis factor (TNF)alpha release from lipopolysaccharide (LPS)-stimulated human monocytes. An intensive programme of work exploring the biology, toxicity and physical chemistry of a novel series of inhibitors, derived from RPR132331, has led to the identification of RPR200765A, a development candidate for the treatment of rheumatoid arthritis (RA). RPR200765A is a potent and selective inhibitor of p38 MAP kinase (IC50 = 50 nM).

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There is circumstantial evidence implicating the pro-inflammatory cytokine tumour necrosis factor (TNF) in the pathogenesis of multiple sclerosis (MS), but there is no direct evidence that TNF can produce demyelination in the central nervous system (CNS). We demonstrate here that single injections of TNF into the dorsal columns of adult rats produced a mild inflammatory response indistinguishable from that seen in control cords, but did not induce demyelination. A similar response was seen when TNF-alpha was injected into dorsal columns where central axons had been remyelinated by Schwann cells.

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Experimental autoimmune neuritis (EAN) is an animal model of Guillain-Barré syndrome. We have shown recently that BB-1101, a broad-spectrum matrix metalloproteinase (MMP) inhibitor, prevents development of EAN when given from the day of immunization and, more important clinically, reduces disease severity when given from symptom onset. This suggests the involvement of MMP activity in the pathogenesis of EAN.

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