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This article looks behind the scenes at the notational and interpretative issues arising from the compositional and rehearsal processes embodied in the Second String Quartet by Michael Finnissy, written for the Kreutzer Quartet in 2006-07. The relationship between the individual parts and corporate whole, as represented by the score, or quasiscore, or even the absence of a score, has been of central importance in all of Finnissy's quartet music to date. Recorded evidence from the rehearsal of the piece is evaluated from both 'insider' and 'outsider' perspectives to demonstrate the extent to which players need to devise new interpretative strategies in response to the specific demands of the notation. Examination of composer-performer interactions reveals how the limits of notation can provide creative tension and imaginative interpretation that contribute to a developing contemporary performance practice.

This article explores the notion of artistic collaboration between performer and composer, a topic that has attracted some attention but whose methodology might be thought to preclude objective discussion by the participants themselves. Although our report can make no claims to objectivity either, it attempts a critical reflection on a specific collaboration between the two authors as composer and performer, respectively. Cast in a dialogical format, it traces the genesis of a composition by Fabrice Fitch for speaking cellist, Per Serafino Calbarsi II: Le Songe de Panurge, written in 2002–3 and premiered in London in October 2006. The collaboration first evolved as a constant exchange of ideas in which concept, technique, and realization were held in fine balance. The piece engages a variety of frames of reference. If its stance in relation to the instrument clearly draws on certain contemporary traditions, for example Lachenmann’s musiqueconcrète instrumentale, other aspects draw on earlier idioms, notably a specialized instance of scordatura, and the use of a spoken text (from the third book of Rabelais’s Pantagruel) that recalls Marin Marais’s Tableau de l’opération de la taille. The interferences and resonances between these influences pose aesthetic questions that are explored within the piece and its performance, while remaining open for the analyst and audience. Finally, the ‘extended techniques’ employed posed specific notational problems. The resulting score navigates a path between tablature and ‘traditional’ notation, in which the emphasis between what is heard and what is played shifts constantly. This hybrid status, we imagine, constitutes a challenge not only for the performer, but for the analyst as well.

Several classical recordings, including \"Beethoven: Quatuors a cordes, op.59 no.3 and op.74\" by the Quatuor Turner and \"Mendelssohn: String quartets, opp.12 and 13\" by the Quatuor Mosaiques, are reviewed.

Plasmodium berghei-infected mice, a well-recognized model of experimental cerebral malaria (ECM), exhibit a systemic inflammatory response. Most investigators hypothesize that leukocytes bind to endothelial cells via intercellular adhesion molecule 1 (ICAM-1), which causes endothelial damage, increased microvascular permeability, and, ultimately, death. ICAM-1 -deficient mice on an ECM-susceptible C57BL/6 background were significantly (p = .04) protected from P. berghei mortality compared with ICAM-1 intact controls. ICAM-1 expression assessed by the dual radiolabeled monoclonal antibody technique was increased in the brain and lung in C57BL/6 mice on day 6 of P. berghei infection compared with uninfected controls (5.3-fold, p = .0003 for brain and 1.8-fold, p = .04 for lung). The increase in ICAM-1 expression coincided with significant (p < .05) increases in microvascular permeability in the brain and lung. In contrast to the hypothesized role for ICAM-1, in vivo analysis by intravital microscopy of leukocyte rolling and adhesion in brain microvasculature of mice revealed markedly increased levels of leukocyte rolling and adhesion in ICAM-1-deficient mice on day 6 of P. berghei infection compared with uninfected controls. In addition, ICAM-1 expression and microvascular permeability were increased in infected ECM-resistant BALB/c mice compared with uninfected BALB/c controls. These results collectively indicate that although ICAM-1 contributes to the mortality of experimental malaria, it is not sufficient for the development of severe experimental malaria. In addition, ICAM-1 expressed on the endothelium or on leukocytes is not required for leukocyte rolling or adhesion to the brain microvasculature of mice during P. berghei malaria. Leukocyte rolling and adhesion in the brain vasculature during P berghei malaria use different ligands than observed during inflammation in other vascular beds.

SummaryThe objectives of this study were to quantify colonic cytokine and endothelial cell adhesion molecule (ECAM) expression in the colons of severe combined immunodeficient (SCID) mice reconstituted with different subsets of CD4+ T lymphocytes. We found that animals injected with CD45RBhigh but not CD45RBlow T cells or phosphate-buffered saline (PBS) developed clinical evidence of colitis at 6-8 weeks following reconstitution, as assessed by loss of body weight, development of loose stools and/or diarrhea, and histopathology. Concurrent with the onset of distal bowel inflammation was enhanced expression of a variety of Thl and macrophage-derived cytokines including interferon γ, tumor necrosis factor-α, interleukin (IL)-1β, IL-6, IL-12, and IL-18 lymphotoxin-β. In addition, message levels and vascular surface expression of ICAM-1, VCAM-1, and MAdCAM-1 were all significantly enhanced in the colitic SCID mice reconstituted with CD45RBhigh T cells compared with SCID mice reconstituted with PBS or CD45RBlow T cells that did not develop disease. Significant increases in some of these ECAMs were also noted in the cecum and stomach and to a lesser degree in the small bowel. Our data confirm that reconstitution of SCID mice with CD45RBhigh but not CD45RBlow T cells induces chronic colitis, and that the colonic inflammation is associated with enhanced expression of proinflammatory cytokines and different ECAMs in the colon. Furthermore, our studies demonstrate that reconstitution of SCID mice with CD45RBhigh T cells enhances ECAM expression in tissues distant from the site of active inflammation.

Plasmodium berghei-infected mice, a well-recognized model of experimental cerebral malaria (ECM), exhibit a systemic inflammatory response. Most investigators hypothesize that leukocytes bind to endothelial cells via intercellular adhesion molecule 1 (ICAM-1), which causes endothelial damage, increased microvascular permeability, and, ultimately, death. ICAM-1-deficient mice on an ECM-susceptible C57BL/6 background were significantly (p = .04) protected from P. berghei mortality compared with ICAM-1 intact controls. ICAM-1 expression assessed by the dual radiolabeled monoclonal antibody technique was increased in the brain and lung in C57BL/6 mice on day 6 of P. berghei infection compared with uninfected controls (5.3-fold, p = .0003 for brain and 1.8-fold, p = .04 for lung). The increase in ICAM-1 expression coincided with significant (p < .05) increases in microvascular permeability in the brain and lung. In contrast to the hypothesized role for ICAM-1, in vivo analysis by intravital microscopy of leukocyte rolling and adhesion in brain microvasculature of mice revealed markedly increased levels of leukocyte rolling and adhesion in ICAM-1-deficient mice on day 6 of P. berghei infection compared with uninfected controls. In addition, ICAM-1 expression and microvascular permeability were increased in infected ECM-resistant BALB/c mice compared with uninfected BALB/c controls. These results collectively indicate that although ICAM-1 contributes to the mortality of experimental malaria, it is not sufficient for the development of severe experimental malaria. In addition, ICAM-1 expressed on the endothelium or on leukocytes is not required for leukocyte rolling or adhesion to the brain microvasculature of mice during P. berghei malaria. Leukocyte rolling and adhesion in the brain vasculature during P. berghei malaria use different ligands than observed during inflammation in other vascular beds.

The objectives of this study were to quantify colonic cytokine and endothelial cell adhesion molecule (ECAM) expression in the colons of severe combined immunodeficient (SCID) mice reconstituted with different subsets of CD4+ T lymphocytes. We found that animals injected with CD45RBhigh but not CD45RBlow T cells or phosphate‐buffered saline (PBS) developed clinical evidence of colitis at 6‐8 weeks following reconstitution, as assessed by loss of body weight, development of loose stools and/or diarrhea, and histopathology. Concurrent with the onset of distal bowel inflammation was enhanced expression of a variety of Thl and macrophage‐derived cytokines including interferon γ, tumor necrosis factor‐α, interleukin (IL)‐1β, IL‐6, IL‐12, and IL‐18 lymphotoxin‐β. In addition, message levels and vascular surface expression of ICAM‐1, VCAM‐1, and MAdCAM‐1 were all significantly enhanced in the colitic SCID mice reconstituted with CD45RBhigh T cells compared with SCID mice reconstituted with PBS or CD45RBlow T cells that did not develop disease. Significant increases in some of these ECAMs were also noted in the cecum and stomach and to a lesser degree in the small bowel. Our data confirm that reconstitution of SCID mice with CD45RBhigh but not CD45RBlow T cells induces chronic colitis, and that the colonic inflammation is associated with enhanced expression of proinflammatory cytokines and different ECAMs in the colon. Furthermore, our studies demonstrate that reconstitution of SCID mice with CD45RBhigh T cells enhances ECAM expression in tissues distant from the site of active inflammation.