Combatting sectarianism from the ground up: The Northern Irish Green and White Army and the football carnival

This paper draws upon participant observation data conducted before and after all 10 qualifying matches for the 2016 UEFA European Football Championship to explore the dynamics underpinning the Northern Irish Green and White Army (GAWA) football carnival. Supplemented by interviews with Northern Ireland fans themselves and informed by the dramaturgical perspectives of Erving Goffman, the paper contends that the anti-sectarian ‘norms’ of GAWA football fandom are dominant in public spaces before matches when the GAWA ‘performance team’ are visible to one another and their audience within a geographically circumscribed space. In a post-match evening context however, various ‘cliques’ of supporters enact their own social rules within a ‘back-stage’ environment of more relaxed peer-to-peer surveillance. These at times transgress the established norms of GAWA fan behaviour. The paper acknowledges that inappropriate supporter behaviour, even within small groups, can damage the wider image of football teams and their supporters in ‘impression management’ terms. But rather than imposing top-down ‘solutions’ which are often devised with limited input from supporters, we suggest that football governing bodies, associations and clubs should look to work in partnership with supporters to identify creative ways in which supporters can be resourced to proactively become ‘norm entrepreneurs’ and challenge inappropriate behaviour from within

Self-Care in the Twenty First Century: A Vital Role for the Pharmacist

<p><b>Article full text</b></p> <p><br></p> <p>The full text of this article can be found here<b>. </b><a href="https://link.springer.com/article/10.1007/s12325-016-0395-5">https://link.springer.com/article/10.1007/s12325-016-0395-5</a></p><p></p> <p><br></p> <p><b>Provide enhanced content for this article</b></p> <p><br></p> <p>If you are an author of this publication and would like to provide additional enhanced content for your article then please contact <a href="http://www.medengine.com/Redeem/”mailto:[email protected]”"><b>[email protected]</b></a>.</p> <p><br></p> <p>The journal offers a range of additional features designed to increase visibility and readership. All features will be thoroughly peer reviewed to ensure the content is of the highest scientific standard and all features are marked as ‘peer reviewed’ to ensure readers are aware that the content has been reviewed to the same level as the articles they are being presented alongside. Moreover, all sponsorship and disclosure information is included to provide complete transparency and adherence to good publication practices. This ensures that however the content is reached the reader has a full understanding of its origin. No fees are charged for hosting additional open access content.</p> <p><br></p> <p>Other enhanced features include, but are not limited to:</p> <p><br></p> <p>• Slide decks</p> <p>• Videos and animations</p> <p>• Audio abstracts</p> <p>• Audio slides</p

Potential Mechanisms of Tumor Cell Killing Employed by <i>WR-delB18R</i>

<div><p>(A) Immunocompetent (C57/B6) mice bearing subcutaneous CMT-93 tumors and treated with a single tail vein injection of 1 × 10⁸ PFU of either psoralen-UV–inactivated WR (IAVV), WR, or <i>WR-delB18R</i> were sacrificed 7 d post-treatment, and CD4-positive cells in tumor sections were scored blind by a pathologist. Average numbers of positive cells per high-powered field (40×) from an average of ten randomly chosen fields from each of three mice treated under each condition are represented (<i>p</i> = 0.035 for IAVV compared to <i>WR-delB18R</i> treated). An asterisk (*) indicates significantly different counts.</p> <p>(B) Mice treated as in <a href="http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0040353#pmed-0040353-g003" target="_blank">Figure 3</a>C and displaying complete responses were rechallenged with a subcutaneous injection of 5 × 10⁵ CMT-93 cells. Tumor burden was measured by calipers (<i>n</i> = 8 mice).</p> <p>(C) Mice (C57/B6 bearing subcutaneous CMT-93 tumors) were treated with a single tail vein injection of 1 × 10⁸ PFU of <i>WR-delB18R</i> virus and sacrificed after 24 h. Tumor sections stained for viral coat proteins indicated initial infection of tumor vascular endothelial cells (top), whereas tumors from mice treated as above, but with <i>WR-delB18R</i> expressing GFP (WR-ΔB18RΔTK-GFP), were examined by immunofluorescence following staining with PE-conjugated antibody targeting CD31 (endothelial cells) (bottom; green = viral GFP expression; red = endothelial cell CD31 staining).</p> <p>(D) Vascular collapse in tumors of mice treated with <i>WR-delB18R</i>. Subcutaneous CMT-93 tumors implanted into C57/B6 mice were examined by ultrasound immediately prior to (left) and 48 h after (right) intravenous treatment with 1 × 10⁸ PFU <i>WR-delB18R</i>. A nonspecific contrast agent was delivered intravenously during ultrasound data acquisition in order to detect tumor vasculature (green); the border of the tumor was manually delineated (red).</p></div

Systemic Delivery, Selectivity, and Oncolytic Activity of <i>WR-delB18R</i> Virus

<div><p>(A) Immunocompetent (BALB/c) mice bearing JC tumors were treated via a single tail vein injection with 1 × 10⁸ PFU of vaccinia strains WR or <i>WR-delB18R</i>. Viral titer (PFU/g) in indicated tissues was determined by plaque assay after sacrifice of animals at indicated time points (<i>n</i> = 3 animals/time point).</p> <p>(B) Immunohistochemistry staining for vaccinia coat proteins in tumor tissue sections of animals treated as above and sacrificed 24 h after viral treatment (magnification 40×).</p> <p>(C) Survival of immunocompetent mice (C57/B6) bearing subcutaneous CMT-93 tumors and treated when tumors reached 50–100 mm³ with a single intratumoral (left) or intravenous (right) injection of <i>WR-delB18R</i> or PBS. Doses of 1 × 10⁴ (circles), 1 × 10⁶ (diamonds), or 1 × 10⁸ (triangles) PFU of virus or PBS controls (squares) were used (<i>n</i> = 5 mice/group; <i>p</i> = 0.0047 for intravenous injections).</p></div

In Vivo Testing, Biodistribution, and Efficacy of <i>JX-795</i>

<div><p>(A) mIFN-β levels were determined by ELISA in the serum, and the tumors of animals (BALB/c bearing subcutaneous JC tumors) treated with (1 × 10⁸ PFU) <i>JX-795</i> (ΔB18RΔTK-IFNb), ΔB18RΔTK virus, or PBS 72 h earlier (<i>n</i> = 3/group).</p> <p>(B) Biodistribution of viral gene expression (as determined by bioluminescence imaging of mice treated with viruses expressing luciferase). Mice (BALB/c) bearing subcutaneous JC tumors (arrows) were treated with a single tail vein injection of 1 × 10⁸ PFU of viruses, <i>TK</i>-deleted (ΔTK-luc; squares), ΔB18RΔTK-luc (triangles), or ΔB18RΔTK-luc-IFNb (<i>JX-795</i>; circles), and imaging performed after luciferin addition. Representative images were taken at 72 h post-treatment. Bioluminescence was quantified over the tumor and the torso of the treated animals (<i>n</i> = 3/group) at times post-treatment (middle and bottom right-hand panels; symbols are for both graphs).</p> <p>(C) Survival curves of BALB/c mice bearing subcutaneous JC tumors and treated with a single tail vein injection of 1 × 10⁸ PFU of ΔB18RΔTK virus (diamonds), ΔB18RΔTK-IFNb (<i>JX-795</i>; triangles) or PBS (squares) (<i>p</i> = 0.028 for ΔB18RΔTK relative to ΔB18RΔTK-IFNb).</p></div

Infection of Primary Tumor and Normal Explant Tissues with <i>B18R-</i> and <i>TK</i>- Deleted Virus Expressing GFP

<p>Three tissue samples (top: rectal tumor with normal rectal tissue; middle: colon tumor metastases in liver; and bottom: endometrial tumor [no normal tissue available]:) are represented. Tumor and normal tissue were mixed with virus, washed, and images taken 48 h later.</p

Additional file 3: Figure S3. of Spatial and temporal epithelial ovarian cancer cell heterogeneity impacts Maraba virus oncolytic potential

Validation of LDLR knockdown using two independent siRNAs. a. iOvCa147-F8 cells were seeded at 20,000 cells per well of a 48-well dish, then transfected with each siLDLR siRNA or siNT control for 48 h. Transfected cells were harvested for protein lysis to perform western blotting for LDLR expression. b. Cells transfected with siLDLR-1, siLDLR-2, or siNT, were infected with MRBV at an MOI of 0.05 for 48 h and viability was measured using CellTiter-Glo®. (PPTX 85 kb

Effect of Type-I IFN on Replication of Vaccinia Strains in Tumor and Normal Cell Lines

<div><p>(A) Primary human cell lines (SAECs and NHBEs) were grown to 50% confluence in six-well plates and treated with human IFN-α (50 U/ml) either 24 h prior to or 5 h after infection with vaccinia (or else PBS was used as a control). Vaccinia strains WR (white bars) or <i>WR-delB18R</i> (WR with deletion of the <i>B18R</i> gene; black bars) were used at an MOI of 1.0 PFU/cell. After 72 h, viral titers in the wells were determined by plaque assay (Student <i>t</i>-test for WR versus <i>WR-delB18R</i> with IFN treatment postinfection, <i>p</i> = 0.0055 for SAECs and 0.0012 for NHBEs).</p> <p>(B) This assay was repeated using human tumor cell lines C33A, A2780, and HCT 116.</p> <p>(C) Serial dilutions of vaccinia strains were added to cells (NHBE or A2780) 5 h before addition of human IFN-alpha (or PBS) as before. Cell viability in the different wells was determined 72 h later by MTS assay, and EC50 values (viral PFU/ml required to reduce cell viability to 50% of untreated well) were determined.</p> <p>An asterisk (*) indicates significant difference (<i>p</i> = 0.0055 for SAECs and 0.0012 for NHBEs).</p></div

In Vitro Testing of <i>JX-795</i> (Western Reserve Vaccinia Virus Containing Deletions of <i>B18R</i> and <i>Thymidine Kinase</i> Genes and Expressing Luciferase and mIFN-β)

<div><p>(A) mIFN-β production following infection of human A2780 cells with <i>JX-795</i> at an MOI of 5.0. IFN-β secretion into the medium during each hour postinfection (up to 14 h) was determined by ELISA.</p> <p>(B) Replication of <i>JX-795</i> (solid symbols and lines; ΔB18RΔTK-IFNb) and an equivalent virus (<i>B18R</i>- and <i>TK</i>-deleted, expressing luciferase only; Δ18ΔTK: open symbols; dashed lines) following infection of murine tumor (CMT-64 [squares] and JC [diamonds]) or nontransformed (NIH 3T3; triangles) cells at an MOI of 1.0.</p> <p>(C) Viral gene expression (luciferase) as measured by bioluminescence 24 h after infection of indicated cell lines with indicated viruses at an MOI of 1.0, and quantified (average of three experiments).</p></div

BN of social dimensions and Strength of influence.

<p>BN of social dimensions and Strength of influence.</p