A method-based approach to historical violin playing: performance practice from a contemporary perspective

Though learning a historical instrument is becoming more and more common among trained violinists, there are few method books that provide detailed instruction. This dissertation is intended to supply violin students with a structured method in historical violin playing that combines information from both historical treatises and contemporary systems of pedagogy. This will enable the student to learn about the historical sources while keeping a sound approach to healthy movement. By looking at source readings from violin methods and other historical sources of the seventeenth and eighteenth century, the student is introduced to historical performance practice. These readings are categorized by the technical information they contain such as violin hold, bow hold, or a certain bow stroke. They are then analyzed and compared to readings by modern pedagogues such as Paul Rolland, Ivan Galamian, Simon Fischer but also experts within the field of Alexander Technique and Body Mapping to enable the student to draw their own conclusions on the techniques they intend to use. To facilitate the process of learning, the author has provided facsimile excerpts both from violin repertoire and historical methods, as well as suggested further practicing material and readings from both historical and modern sources

CD25(bright)CD4(+ )regulatory T cells are enriched in inflamed joints of patients with chronic rheumatic disease

CD25(+)CD4(+ )regulatory T cells participate in the regulation of immune responses. We recently demonstrated the presence of CD25(bright)CD4(+ )regulatory T cells with a capacity to control T cell proliferation in the joints of patients with rheumatoid arthritis. Here, we investigate a possible accumulation of these regulatory T cells in the inflamed joint of different rheumatic diseases including rheumatoid arthritis. The studies are also extended to analyze whether cytokine production can be suppressed by the regulatory T cells. Synovial fluid and peripheral blood samples were obtained during relapse from 36 patients with spondyloarthropathies, 21 adults with juvenile idiopathic arthritis and 135 patients with rheumatoid arthritis, and the frequency of CD25(bright)CD4(+ )T cells was determined. Of 192 patients, 182 demonstrated a higher frequency of CD25(bright)CD4(+ )T cells in synovial fluid than in peripheral blood. In comparison with healthy subjects, the patients had significantly fewer CD25(bright)CD4(+ )T cells in peripheral blood. For functional studies, synovial fluid cells from eight patients were sorted by flow cytometry, and the suppressive capacity of the CD25(bright)CD4(+ )T cells was determined in in vitro cocultures. The CD25(bright)CD4(+ )T cells suppressed the production of both type 1 and 2 cytokines including interleukin-17, as well as proliferation, independently of diagnosis. Thus, irrespective of the inflammatory joint disease investigated, CD25(bright)CD4(+ )T cells were reduced in peripheral blood and enriched in the joint, suggesting an active recruitment of regulatory T cells to the affected joint. Their capacity to suppress both proliferation and cytokine secretion might contribute to a dampening of local inflammatory processes

Differential effects on BAFF and APRIL levels in rituximab-treated patients with systemic lupus erythematosus and rheumatoid arthritis

The objective of this study was to investigate the interaction between levels of BAFF (B-cell activation factor of the tumour necrosis factor [TNF] family) and APRIL (a proliferation-inducing ligand) and B-cell frequencies in patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) treated with the B-cell-depleting agent rituximab. Ten patients with SLE were treated with rituximab in combination with cyclophosphamide and corticosteroids. They were followed longitudinally up to 6 months after B-cell repopulation. Nine patients with RA, resistant or intolerant to anti-TNF therapy, treated with rituximab plus methotrexate were investigated up to 6 months after treatment. The B-cell frequency was determined by flow cytometry, and serum levels of BAFF and APRIL were measured by enzyme-linked immunosorbent assays. BAFF levels rose significantly during B-cell depletion in both patient groups, and in patients with SLE the BAFF levels declined close to pre-treatment levels upon B-cell repopulation. Patients with SLE had normal levels of APRIL at baseline, and during depletion there was a significant decrease. In contrast, patients with RA had APRIL levels 10-fold higher than normal, which did not change during depletion. At baseline, correlations between levels of B cells and APRIL, and DAS28 (disease activity score using 28 joint counts) and BAFF were observed in patients with RA. In summary, increased BAFF levels were observed during absence of circulating B cells in our SLE and RA patient cohorts. In spite of the limited number of patients, our data suggest that BAFF and APRIL are differentially regulated in different autoimmune diseases and, in addition, differently affected by rituximab treatment