The Penny’s Dropped: Renegotiating the contemporary coin deposit

This is the Accepted Manuscript of the following article: Ceri Houlbrook, “The penny’s dropped: Renegotiating the contemporary coin deposit”, Journal of Material Culture, Vol. 20(2): 173-189, March 2015. The final published version is available at: http://journals.sagepub.com/doi/pdf/10.1177/1359183515577120#articleCitationDownloadContainer © 2015, © SAGE Publications.This article examines the status of coins as contemporary deposits in the British Isles. With a focus on both historical and contemporary sites, from the Neolithic long barrow of Wayland’s Smithy, Oxfordshire, to the plethora of wishing-wells and coin-trees distributed across the British Isles, it demonstrates the popularity of coins as ritual deposits. The author considers how they are perceived and treated by site custodians, and concludes with a case study of an archaeological excavation, the 2013 Ardmaddy Wishing-Tree Project, which recovered a large amount of contemporary coin deposits. This article does not aim to locate itself within the debates of site custodianship and accessibility, nor does it propose to address the broader dilemmas of a site’s ritual continuity or resurgence. Instead, its aim is to encourage archaeologists to consider the contemporary deposit as an integral part of the ritual narrative of a site, rather than as disposable ‘ritual litter’.Peer reviewedFinal Accepted Versio

Alterations of renal phenotype and gene expression profiles due to protein overload in NOD-related mouse strains

BACKGROUND: Despite multiple causes, Chronic Kidney Disease is commonly associated with proteinuria. A previous study on Non Obese Diabetic mice (NOD), which spontaneously develop type 1 diabetes, described histological and gene expression changes incurred by diabetes in the kidney. Because proteinuria is coincident to diabetes, the effects of proteinuria are difficult to distinguish from those of other factors such as hyperglycemia. Proteinuria can nevertheless be induced in mice by peritoneal injection of Bovine Serum Albumin (BSA). To gain more information on the specific effects of proteinuria, this study addresses renal changes in diabetes resistant NOD-related mouse strains (NON and NOD.B10) that were made to develop proteinuria by BSA overload. METHODS: Proteinuria was induced by protein overload on NON and NOD.B10 mouse strains and histology and microarray technology were used to follow the kidney response. The effects of proteinuria were assessed and subsequently compared to changes that were observed in a prior study on NOD diabetic nephropathy. RESULTS: Overload treatment significantly modified the renal phenotype and out of 5760 clones screened, 21 and 7 kidney transcripts were respectively altered in the NON and NOD.B10. Upregulated transcripts encoded signal transduction genes, as well as markers for inflammation (Calmodulin kinase beta). Down-regulated transcripts included FKBP52 which was also down-regulated in diabetic NOD kidney. Comparison of transcripts altered by proteinuria to those altered by diabetes identified mannosidase 2 alpha 1 as being more specifically induced by proteinuria. CONCLUSION: By simulating a component of diabetes, and looking at the global response on mice resistant to the disease, by virtue of a small genetic difference, we were able to identify key factors in disease progression. This suggests the power of this approach in unraveling multifactorial disease processes

Use of intervention mapping to adapt a health behavior change intervention for endometrial cancer survivors: The shape-up following cancer treatment program

Background: About 80% of endometrial cancer survivors (ECS) are overweight or obese and have sedentary behaviors. Lifestyle behavior interventions are promising for improving dietary and physical activity behaviors, but the constructs associated with their effectiveness are often inadequately reported. The aim of this study was to systematically adapt an evidence-based behavior change program to improve healthy lifestyle behaviors in ECS. Methods: Following a review of the literature, focus groups and interviews were conducted with ECS (n = 16). An intervention mapping protocol was used for the program adaptation, which consisted of six steps: a needs assessment, formulation of matrices of change objectives, selection of theoretical methods and practical applications, program production, adoption and implementation planning, and evaluation planning. Social Cognitive Theory and Control Theory guided the adaptation of the intervention. Results: The process consisted of eight 90-min group sessions focusing on shaping outcome expectations, knowledge, self-efficacy, and goals about healthy eating and physical activity. The adapted performance objectives included establishment of regular eating, balanced diet, and portion sizes, reduction in sedentary behaviors, increase in lifestyle and organized activities, formulation of a discrepancy-reducing feedback loop for all above behaviors, and trigger management. Information on managing fatigue and bowel issues unique to ECS were added. Conclusions: Systematic intervention mapping provided a framework to design a cancer survivor-centered lifestyle intervention. ECS welcomed the intervention and provided essential feedback for its adaptation. The program has been evaluated through a randomized controlled trial

TYK2 Kinase Activity Is Required for Functional Type I Interferon Responses In Vivo

Tyrosine kinase 2 (TYK2) is a member of the Janus kinase (JAK) family and is involved in cytokine signalling. In vitro analyses suggest that TYK2 also has kinase-independent, i.e., non-canonical, functions. We have generated gene-targeted mice harbouring a mutation in the ATP-binding pocket of the kinase domain. The Tyk2 kinase-inactive (Tyk2K923E) mice are viable and show no gross abnormalities. We show that kinase-active TYK2 is required for full-fledged type I interferon- (IFN) induced activation of the transcription factors STAT1-4 and for the in vivo antiviral defence against viruses primarily controlled through type I IFN actions. In addition, TYK2 kinase activity was found to be required for the protein’s stability. An inhibitory function was only observed upon over-expression of TYK2K923E in vitro. Tyk2K923E mice represent the first model for studying the kinase-independent function of a JAK in vivo and for assessing the consequences of side effects of JAK inhibitors

Chemical Biology Drug Sensitivity Screen Identifies Sunitinib as Synergistic Agent with Disulfiram in Prostate Cancer Cells

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