Publications by authors named "Craig Ritchie"

Objectives: This was a pilot, phase 2a study to assess methodological feasibility and the safety and efficacy of donepezil in preventing postoperative delirium after elective total hip replacement surgery in older people without pre-existing dementia. The hypothesis was that donepezil would reduce the incidence of postoperative delirium.

Methods: A double blind, placebo controlled, parallel group randomized trial was undertaken.

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Background: The aim of this study was to perform a systematic review and meta-analysis of the literature regarding the incidence of delirium following orthopedic surgery.

Methods: Relevant papers were sourced from online databases and gray literature. Included studies used a validated diagnostic method to measure the incidence of delirium in a prospective sample of adult/elderly orthopedic patients.

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Since the description of the amyloid plaque in the pathology of Alzheimer's disease, one of the main focuses of research has been the role of the amyloid precursor protein metabolite amyloid-beta, which is the constituent protein of plaque. Affecting the production, aggregation or clearance of this protein may well have a modifying effect on disease progression. Although available therapies for Alzheimer's disease may interact with amyloid-beta in vivo, no conspicuous disease-modifying effect has been demonstrated in clinical trials with these drugs.

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The authors estimated the effects of each of the three commonly used drugs for Alzheimer disease (donepezil, galantamine, and rivastigmine) in terms of predefined clinical outcomes and trial completion rates, by dosing level, and described differences among them. Using both electronic and manual search strategies (January 1992 to July 2002), a metaanalysis examined the effect of the drugs on clinical outcomes and completion rates. Regression analyses compared the effect of dose on clinical outcomes and completion rates, using 10 donepezil, 6 galantamine, and 5 rivastigmine articles.

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Background: Alzheimer disease (AD) may be caused by the toxic accumulation of beta-amyloid (Abeta).

Objective: To test this theory, we developed a clinical intervention using clioquinol, a metal-protein-attenuating compound (MPAC) that inhibits zinc and copper ions from binding to Abeta, thereby promoting Abeta dissolution and diminishing its toxic properties.

Methods: A pilot phase 2 clinical trial in patients with moderately severe Alzheimer disease.

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The title compounds, C(15)H(13)NO(4), (I), and C(13)H(9)NO, (II), are produced, along with the corresponding anilines, by the reduction of the appropriate o-nitrobenzophenones. In (I), the planar benzisoxazole and phenol fragments are tilted relative to one another by a rotation of 53.02 (14) degrees about the bond joining them, and the molecules are linked into chains by phenol O--H.

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Background: We aimed to assess why carers seek participation for their relatives in clinical trials of Alzheimer's disease (AD) medications, and to assess carer impressions of the value of trial participation.

Method: A retrospective questionnaire was sent to 31 carers of participants in clinical trials for AD conducted at the Mental Health Research Institute and the National Aging Research Institute between January 1997 and December 1999.

Results: Twenty-five questionnaires (81%) were returned, completed to an extent to permit analysis.

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