234 research outputs found

    Israel and a sports boycott: Antisemitic? Anti-Zionist?

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    The paper identifies and summarises the debates that surround the place of Israel in international sport and assesses how that place is increasingly being contested. The long-standing conflict between Israel and Palestine has begun to manifest in the world of sport with the paper sketching the debates of those calling for, and those opposed to, sport sanctions/boycott of Israel until the ‘Palestinian Question’ is resolved. Five related tasks are addressed: first, to summarise the call for sanctions/boycott emanating from the Boycott, Disinvestment and Sanctions movement. Second, to explore how this call is establishing itself in the world of sport. The responses of those opposed to any form of sanction/boycott are then considered. The confusion that surrounds the term antisemitism is addressed and the relationship between (anti-) Zionism and antisemitism unpacked. The discussion concludes with an assessment of the claim made by the Israeli state, and its supporters, that any action against the country’s participation in international sport would be an act of antisemitism. Offering a timely, integrated summary of the heated debates that surround the Israel/Palestine conflict, the paper contributes to a wider discussion on the relationship between sport and politics

    The Use of Neutralities in International Tax Policy

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    Harmonization guidelines for HLA-peptide multimer assays derived from results of a large scale international proficiency panel of the Cancer Vaccine Consortium

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    PURPOSE: The Cancer Vaccine Consortium of the Cancer Research Institute (CVC-CRI) conducted a multicenter HLA-peptide multimer proficiency panel (MPP) with a group of 27 laboratories to assess the performance of the assay. EXPERIMENTAL DESIGN: Participants used commercially available HLA-peptide multimers and a well characterized common source of peripheral blood mononuclear cells (PBMC). The frequency of CD8+ T cells specific for two HLA-A2-restricted model antigens was measured by flow cytometry. The panel design allowed for participants to use their preferred staining reagents and locally established protocols for both cell labeling, data acquisition and analysis. RESULTS: We observed significant differences in both the performance characteristics of the assay and the reported frequencies of specific T cells across laboratories. These results emphasize the need to identify the critical variables important for the observed variability to allow for harmonization of the technique across institutions. CONCLUSIONS: Three key recommendations emerged that would likely reduce assay variability and thus move toward harmonizing of this assay. (1) Use of more than two colors for the staining (2) collect at least 100,000 CD8 T cells, and (3) use of a background control sample to appropriately set the analytical gates. We also provide more insight into the limitations of the assay and identified additional protocol steps that potentially impact the quality of data generated and therefore should serve as primary targets for systematic analysis in future panels. Finally, we propose initial guidelines for harmonizing assay performance which include the introduction of standard operating protocols to allow for adequate training of technical staff and auditing of test analysis procedures

    Herpesviruses carrying a Brainbow cassette reveal replication and expression of limited numbers of incoming genomes

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    Whether all the infectious herpesvirus particles entering a cell are able to replicate and/or express their genomes is not known. Here, we developed a general method to determine the number of viral genomes expressed in an infected cell. We constructed and analysed fluorophore expression from a recombinant pseudorabies virus (PRV263) carrying a Brainbow cassette (Cre-conditional expression of different fluorophores). Using three isogenic strains derived from PRV263, each expressing a single fluorophore, we analysed the colour composition of cells infected with these three viruses at different multiplicities. We estimate that fewer than seven incoming genomes are expressed per cell. In addition, those templates that are expressed are the genomes selected for replication and packaging into virions. This finite limit on the number of viral genomes that can be expressed is an intrinsic property of the infected cell and may be influenced by viral and cellular factors
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