We tested the feasibility of a computer based at-home testing device (AHTD) in early-stage, unmedicated Parkinson’s disease (PD) patients over 6 months. We measured compliance, technical reliability, and patient satisfaction to weekly assessments of tremor, small and large muscle bradykinesia, speech, reaction/movement times, and complex motor control. relative to the UPDRS motor score. The AHTD is a 6.5 x 10 computerized assessment battery. Data are stored on a USB memory stick and sent by internet to a central data repository as encrypted data packets. Although not designed or powered to measure change, the study collected data to observe patterns relative to UPDRS motor scores. Fifty-two PD patients enrolled, and 50 completed the six month trial, 48 remaining without medication. Patients complied with 90.6% of weekly 30-minute assessments, and 98.5% of data packets were successfully transmitted and decrypted. On a 100-point scale, patient satisfaction with the program at study end was 87.2 (range 80–100). UPDRS motor scores significantly worsened over 6 months, and trends for worsening over time occurred for alternating finger taps (p=.08), tremor (p=.06) and speech (p=.11). Change in tremor was a significant predictor of change in UPDRS (p=0.047) and was detected in the first month of the study. This new computer-based technology offers a feasible format for assessing PD-related impairment from home. The high patient compliance and satisfaction suggest the feasibility of its incorporation into larger clinical trials, especially when travel is difficult and early changes or frequent data collection are considered important to document.

OBJECTIVE -The aim of this study was to determine the effects of fenofibrate (160 mg/day) on fasting and postprandial lipoproteins, oxidized fatty acids, and inflammatory mediators in subjects with hypertriglyceridemia and the metabolic syndrome.RESEARCH DESIGN AND METHODS -Fifty-nine subjects with fasting hypertriglyceridemia (Ն1.7 and Ͻ6.9 mmol/l) and two or more of the Adult Treatment Panel III criteria for the metabolic syndrome were randomly assigned to fenofibrate (160 mg/day) or placebo in a double-blind, controlled clinical trial.RESULTS -Fenofibrate treatment lowered fasting triglycerides (Ϫ46.1%, P Ͻ 0.0001) and postprandial (area under the curve) triglycerides (Ϫ45.4%, P Ͻ 0.0001) due to significant reductions in postprandial levels of large (Ϫ40.8%, P Ͻ 0.0001) and medium (Ϫ49.5%, P Ͻ 0.0001) VLDL particles. The number of fasting total LDL particles was reduced in fenofibratetreated subjects (Ϫ19.0%, P ϭ 0.0033) primarily due to reductions in small LDL particles (Ϫ40.3%, P Ͻ 0.0001); these treatment differences persisted postprandially. Fasting and postprandial oxidized fatty acids were reduced in fenofibrate-treated subjects compared with placebo-administered subjects (Ϫ15.3%, P ϭ 0.0013, and 31.0%, P Ͻ 0.0001, respectively), and fenofibrate therapy lowered fasting and postprandial soluble vascular cell adhesion molecule-1 (VCAM-1) (Ϫ10.9%, P ϭ 0.0005, and Ϫ12.0%, P ϭ 0.0001, respectively) as well as fasting and postprandial soluble intercellular adhesion molecule-1 (ICAM-1) (Ϫ14.8%, P Ͻ 0.0001, and Ϫ15.3%, P Ͻ 0.0001, respectively). Reductions in VCAM-1 and ICAM-1 were correlated with reductions in fasting and postprandial large VLDL particles (P Ͻ 0.0001) as well as postprandial oxidized fatty acids (P Ͻ 0.0005).CONCLUSIONS -Triglyceride-lowering therapy with fenofibrate reduced fasting and postprandial free fatty acid oxidation and inflammatory responses, and these antiatherosclerotic effects were most highly correlated with reductions in large VLDL particles. Diabetes Care 30:1945-1951, 2007T he metabolic syndrome represents an agglomeration of interrelated risk factors that include abnormally high fasting triglyceride levels (1,2). In a recent analysis, hypertriglyceridemia (Ն1.7 mmol/l) represented the component of the metabolic syndrome most strongly associated with a history of myocardial infarction and stroke (3). Furthermore, elevated fasting triglyceride levels (Ն1.4 mmol/l) and an enlarged waist circumference (Ͼ89 cm) were the two characteristics of the metabolic syndrome that were associated with the greatest increased risk for all-cause mortality and cardiovascular deaths among postmenopausal women (4).Hypertriglyceridemia signifies the presence of increased plasma triglycerideremnant lipoproteins, and the concentrations of remnant-like lipoproteins are further enhanced postprandially among hypertriglyceridemic subjects (5). Remnant-like proteins have been shown to increase intracellular oxidant concentrations and lipid peroxide levels in culture media and to activate nuclear factor-B ...

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Over the past decade different approaches to mobilising knowledge inCommunity2University Partnership (CUP) contexts have emerged in the UK. Despite this,detailed accounts of the intricate texture of these approaches, enabling others to replicate orlearn from them, are lacking. This paper adds to the literature which begins to address thisgap. The case considered here concentrates on one particular approach to knowledgemobilisation (KM) developed in the UK context. It provides an account of the authors’involvement in applying the concept, and practical lessons from a community of practice(CoP) approach, to developing knowledge exchange (KE) between academics, parents andpractitioners. The authors’ approach to KM explicitly attempts to combat power differentialsbetween academics and community partners, and problematises knowledge powerhierarchies. The paper explores the CoP concept and critically investigates key elements ofrelevance to developing KE in the CUP context. Specific themes addressed are those ofpower, participation and working across boundaries by CoP members with very differentsubject positions and knowledge capitals. The paper concludes that CoPs can be a usefulmechanism for KM, but have many limitations depending on the specific context in whichKM is being undertaken

The healing of articular surface defects has been studied with conventional histology, which relies on the staining of the extracellular matrix to identify the phenotype of the cells present. A chondrospecific cellular marker would be useful. S-100 protein has been found in all chondroid tissues studied, and we evaluated its usefulness in the study of articular cartilage repair. Full-thickness rabbit femoral condylar defects were made, and the specimens were studied at serial time intervals. S-100 protein staining positively showed chondroid cells in the 7- and 14-day specimens, which were not identifiable by conventional techniques. At 30 and 60 days, an S-100 positive band of cells separated a deep safranin-O positive hypertrophic layer from a fibrocellular surface layer. At 120 days, the presence of S-100 protein identified cells with chondrogenic potential, and the lack of S-100 protein in other cells embedded in conventionally stained matrix suggested that these cells were no longer of a chondroid phenotype. The presence of S-100 protein-identified chondroid cells early in the repair process when the cells had not begun to synthesize conventionally stainable matrix and the lack of S-100 protein in cells late in the repair positively identified a phenotypic change earlier than conventional histology.