Diagnostic reliability of magnetic resonance imaging for central nervous system syndromes in systemic lupus erythematosus: a prospective cohort study

<p>Abstract</p> <p>Background</p> <p>Previous studies of magnetic resonance imaging (MRI) as a diagnostic tool for central nervous system (CNS) syndromes in systemic lupus erythematosus (SLE) contained several limitations such as study design, number of enrolled patients, and definition of CNS syndromes. We overcame these problems and statistically evaluated the diagnostic values of abnormal MRI signals and their chronological changes in CNS syndromes of SLE.</p> <p>Methods</p> <p>We prospectively studied 191 patients with SLE, comparing those with (n = 57) and without (n = 134) CNS syndrome. CNS syndromes were characterized using the American College of Rheumatology case definitions.</p> <p>Results</p> <p>Any abnormal MRI signals were more frequently observed in subjects in the CNS group (n = 25) than in the non-CNS group (n = 32) [relative risk (RR), 1.7; 95% confidence interval (CI), 1.1-2.7; <it>p </it>= 0.016] and the positive and negative predictive values for the diagnosis of CNS syndrome were 42% and 76%, respectively. Large abnormal MRI signals (ø ≥ 10 mm) were seen only in the CNS group (n = 7; RR, 3.7; CI, 2.9-4.7; <it>p </it>= 0.0002), whereas small abnormal MRI signals (ø < 10 mm) were seen in both groups with no statistical difference. Large signals always paralleled clinical outcome (<it>p </it>= 0.029), whereas small signals did not (<it>p </it>= 1.000).</p> <p>Conclusions</p> <p>Abnormal MRI signals, which showed statistical associations with CNS syndrome, had insufficient diagnostic values. A large MRI signal was, however, useful as a diagnostic and surrogate marker for CNS syndrome of SLE, although it was less common.</p

Measuring capacity building in communities: a review of the literature

<p>Abstract</p> <p>Background</p> <p>Although communities have long been exhorted to make efforts to enhance their own health, such approaches have often floundered and resulted in little or no health benefits when the capacity of the community has not been adequately strengthened. Thus being able to assess the capacity building process is paramount in facilitating action in communities for social and health improvement. The current review aims to i) identify all domains used in systematically documented frameworks developed by other authors to assess community capacity building; and ii) to identify the dimensions and attributes of each of the domains as ascribed by these authors and reassemble them into a comprehensive compilation.</p> <p>Methods</p> <p>Relevant published articles were identified through systematic electronic searches of selected databases and the examination of the bibliographies of retrieved articles. Studies assessing capacity building or community development or community participation were selected and assessed for methodological quality, and quality in relation to the development and application of domains which were identified as constituents of community capacity building. Data extraction and analysis were undertaken using a realist synthesis approach.</p> <p>Results</p> <p>Eighteen articles met the criteria for this review. The various domains to assess community capacity building were identified and reassembled into nine comprehensive domains: "learning opportunities and skills development", "resource mobilization", "partnership/linkages/networking", "leadership", "participatory decision-making", "assets-based approach", "sense of community", "communication", and "development pathway". Six sub-domains were also identified: "shared vision and clear goals", "community needs assessment", "process and outcome monitoring", "sustainability", "commitment to action" and "dissemination".</p> <p>Conclusions</p> <p>The set of domains compiled in this review serve as a foundation for community-based work by those in the field seeking to support and nurture the development of competent communities. Further research is required to examine the robustness of capacity domains over time and to examine capacity development in association with health or other social outcomes.</p

Induction of Selective Blood-Tumor Barrier Permeability and Macromolecular Transport by a Biostable Kinin B1 Receptor Agonist in a Glioma Rat Model

Treatment of malignant glioma with chemotherapy is limited mostly because of delivery impediment related to the blood-brain tumor barrier (BTB). B1 receptors (B1R), inducible prototypical G-protein coupled receptors (GPCR) can regulate permeability of vessels including possibly that of brain tumors. Here, we determine the extent of BTB permeability induced by the natural and synthetic peptide B1R agonists, LysdesArg9BK (LDBK) and SarLys[dPhe8]desArg9BK (NG29), in syngeneic F98 glioma-implanted Fischer rats. Ten days after tumor inoculation, we detected the presence of B1R on tumor cells and associated vasculature. NG29 infusion increased brain distribution volume and uptake profiles of paramagnetic probes (Magnevist and Gadomer) at tumoral sites (T1-weighted imaging). These effects were blocked by B1R antagonist and non-selective cyclooxygenase inhibitors, but not by B2R antagonist and non-selective nitric oxide synthase inhibitors. Consistent with MRI data, systemic co-administration of NG29 improved brain tumor delivery of Carboplatin chemotherapy (ICP-Mass spectrometry). We also detected elevated B1R expression in clinical samples of high-grade glioma. Our results documented a novel GPCR-signaling mechanism for promoting transient BTB disruption, involving activation of B1R and ensuing production of COX metabolites. They also underlined the potential value of synthetic biostable B1R agonists as selective BTB modulators for local delivery of different sized-therapeutics at (peri)tumoral sites

Pericytes from Mesenchymal Stem Cells as a model for the blood-brain barrier

We would like to thank Prof. N. Joan Abbott (Institute of Pharmaceutical Science, King’s College London, UK) for useful suggestions and discussions. We thank National Natural Science Foundation of China (21602003, X.T.) and EPSRC (EP/I001697/1, EP/G062137/1, G.B.) for sponsoring the project