369 research outputs found
The Birsay Bay Project Volume 3: The Brough of Birsay, Orkney: Investigations 1954-2014
The Brough of Birsay was the power-centre of the Viking earldom of Orkney and is one of Historic Environment Scotland’s key monuments and visitor attractions on the islands. This publication is the culmination of 60 years of investigations that took place on the site between 1954 and 2014.
This new volume incorporates comprehensive accounts of work undertaken by Dr Ralegh Radford and Mr Stewart Cruden between 1954 and 1964, excavations by the Viking and Early Settlement Research Project under the direction of the author on site between 1974 and 1981, a rescue excavation in 1993, a geophysical survey in 2007 and archival research up to 2014.
Specialist artefactual and palaeobiological studies of metallurgical material, ogham inscriptions and a gilt-bronze mount of Insular origin are included, together with re-analysis of the radiocarbon dates from all sites in Birsay Bay, and a re-assessment of the architecture and dating of the church and related buildings on the Brough itself.
The final two chapters put the Brough, as both a Pictish power-centre and the hub of the Viking earldom, in the overall context of Birsay Bay and Viking and late Norse Orkney, and the wider world between the Pictish and late Norse/Medieval periods.
As well as being the author’s third and final volume reporting on work for the Birsay Bay Project, this volume completes a trilogy of studies of the Brough itself, alongside Mrs Cecil Curle’s and Prof John Hunter’s earlier monographs
Ogham inscriptions from the Brough of Birsay
Detailed discussion of three ogham-inscribed building slabs excavated from the Brough of Birsay in 1934, 1960, and 1980 respectively. The former two were long thought lost but have recently been identified in the collections of the National Museum of Scotland. The stones are illustrated and readings proposed. It is argued that the inscriptions are likely graffiti, carved while the stones were in situ as constructional elements of a building from the late Pictish or early Norse phases of the site
DMCC55B Dataset Description
These files accompany "The Dual Mechanisms of Cognitive Control dataset, a theoretically-guided within-subject task fMRI battery" (published Dataset Descriptor at https://doi.org/10.1038/s41597-022-01226-4, preprint at https://doi.org/10.1101/2021.05.28.446178) by Joset A. Etzel, Rachel E. Brough, Michael C. Freund, Alexander Kizhner, Yanli Lin, Matthew F. Singh, Rongxiang Tang, Allison Tay, Anxu Wang, and Todd S. Braver. The manuscript describes the DMCC55B dataset, which is available at https://openneuro.org/datasets/ds003465/
Stringent and reproducible tetracycline-regulated transgene expression by site-specific insertion at chromosomal loci with pre-characterised induction characteristics
Background: The ability to regulate transgene expression has many applications, mostly concerning the analysis of gene function. Desirable induction characteristics, such as low un-induced expression, high induced expression and limited cellular heterogeneity, can be seriously impaired by chromosomal position effects at the site of transgene integration. Many clones may therefore need to be screened before one with optimal induction characteristics is identified. Furthermore, such screens must be repeated for each new transgene investigated, and comparisons between clones with different transgenes is complicated by their different integration sites. Results: To circumvent these problems we have developed a "screen and insert" strategy in which clones carrying a transgene for a fluorescent reporter are first screened for those with optimal induction characteristics. Site-specific recombination (SSR) is then be used repeatedly to insert any new transgene at the reporter transgene locus of such clones so that optimal induction characteristics are conferred upon it. Here we have tested in a human fibrosarcoma cell line (HT1080) two of many possible implementations of this approach. Clones (e. g. Rht14-10) in which a GFP reporter gene is very stringently regulated by the tetracycline (tet) transactivator (tTA) protein were first identified flow-cytometrically. Transgenes encoding luciferase, I-SceI endonuclease or Rad52 were then inserted by SSR at a LoxP site adjacent to the GFP gene resulting stringent tet-regulated transgene expression. In clone Rht14-10, increases in expression from essentially background levels (+ tet) to more than 10(4)-fold above background (-tet) were reproducibly detected after Cre-mediated insertion of either the luciferase or the I-SceI transgenes. Conclusion: Although previous methods have made use of SSR to integrate transgenes at defined sites, none has effectively combined this with a pre- selection step to identify integration sites that support optimal regulatory characteristics. Rht14-10 and similar HT1080-derived clones can now be used in conjunction with a convenient delivery vector (pIN2-neoMCS), in a simple 3-step protocol leading to stringent and reproducible transgene regulation. This approach will be particularly useful for transgenes whose products are very active at low concentrations and/or for comparisons of multiple related transgenes
Terminus Traces for publication 'Ocean-forcing and glacier-specific factors drive differing glacier response across the 69 oN boundary, east Greenland' (Version 1)
<p>Dataset supporting publication 'Brough, S., Carr, J.R., Ross, N., Lea, J.M. (2023) Ocean-forcing and glacier-specific factors drive differing glacier response across the 69 <sup>o</sup>N boundary, east Greenland. J. Geophys. Res. Earth Surf. <a href="https://doi.org/10.1029/2022JF006857">https://doi.org/10.1029/2022JF006857</a>.'</p>
<p>This dataset provides GIS ready shapefiles of mapped terminus traces for 24 east Greenland glaciers between 2013 and 2020 for the aforementioned publication. Data are provided in both geographic (EPSG: 4326; WGS84) and projected (EPSG:3413; NSIDC Sea Ice Polar Stereographic North) coordinate systems. As each terminus trace has metadata appended, including the unique path identifier, it is possible to directly and easily identify the original image used in the mapping process. Both shapefiles are compatible for ingestion into the Google Earth Digitisation Tool (GEEDiT) Reviewer (<a href="https://liverpoolgee.wordpress.com/">https://liverpoolgee.wordpress.com/</a>) for reviewing and sub-setting the dataset (see Lea, J.M. [2018] Earth Surf. Dynam. 6, 551–561. <a href="https://doi.org/10.5194/esurf-6-551-2018">https://doi.org/10.5194/esurf-6-551-2018</a>).</p>
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<p>When using this data product in a publication, please include the following citations:</p>
<p>Brough, S., Carr, J.R., Ross, N., Lea, J.M. (2023). Terminus Traces for publication 'Ocean-forcing and glacier-specific factors drive differing glacier response across the 69 <sup>o</sup>N boundary, east Greenland' (Version 1) [Data set]. Zenodo. <a href="https://doi.org/10.5281/zenodo.6904219">https://doi.org/10.5281/zenodo.6904219</a>.</p>
<p>Brough, S., Carr, J.R., Ross, N., Lea, J.M. (2023) Ocean-forcing and glacier-specific factors drive differing glacier response across the 69 <sup>o</sup>N boundary, east Greenland. J. Geophys. Res. Earth Surf. <a href="https://doi.org/10.1029/2022JF006857">https://doi.org/10.1029/2022JF006857</a>.</p>
On vanishing class sizes in finite groups
Let G be a finite group. An element g of G is called a vanishing element if there exists an irreducible character χ of G such that χ(g)=0; in this case, we say that the conjugacy class of g is a vanishing conjugacy class. In this paper, we discuss some arithmetical properties concerning the sizes of the vanishing conjugacy classes in a finite group
Author response to : Brough et al. in response to\ud the recently published article : Lottering,N., MacGregor,D.M.,Barry,M.D.,Reynolds,M.S., Gregory,L.S., 2014. Introducing standardized protocols for anthropological measurement of virtual sub-adult crania using computed tomography 2(1),34–38
Firstly, we would like to thank Ms. Alison Brough and her colleagues for their positive commentary on our published work [1] and their appraisal of our utility of the “off-set plane” protocol for anthropometric analysis. The standardized protocols described in our manuscript have wide applications, ranging from forensic anthropology and paleodemographic research to clinical settings such as paediatric practice and orthopaedic surgical design. We affirm that the use of geometrically based reference tools commonly found in computer aided design (CAD) programs such as Geomagic Design X® are imperative for more automated and precise measurement protocols for quantitative skeletal analysis. Therefore we stand by our recommendation of the use of software such as Amira and Geomagic Design X® in the contexts described in our manuscript..
A HUWE1 defect causes PARP inhibitor resistance by modulating the BRCA1-∆11q splice variant
Abstract Although PARP inhibitors (PARPi) now form part of the standard-of-care for the treatment of homologous recombination defective cancers, de novo and acquired resistance limits their overall effectiveness. Previously, overexpression of the BRCA1-∆11q splice variant has been shown to cause PARPi resistance. How cancer cells achieve increased BRCA1-∆11q expression has remained unclear. Using isogenic cells with different BRCA1 mutations, we show that reduction in HUWE1 leads to increased levels of BRCA1-∆11q and PARPi resistance. This effect is specific to cells able to express BRCA1-∆11q (e.g. BRCA1 exon 11 mutant cells) and is not seen in BRCA1 mutants that cannot express BRCA1-∆11q, nor in BRCA2 mutant cells. As well as increasing levels of BRCA1-∆11q protein in exon 11 mutant cells, HUWE1 silencing also restores RAD51 nuclear foci and platinum salt resistance. HUWE1 catalytic domain mutations were also seen in a case of PARPi resistant, BRCA1 exon 11 mutant, high grade serous ovarian cancer. These results suggest how elevated levels of BRCA1-∆11q and PARPi resistance can be achieved, identify HUWE1 as a candidate biomarker of PARPi resistance for assessment in future clinical trials and illustrate how some PARPi resistance mechanisms may only operate in patients with particular BRCA1 mutations.Cancer Research UK https://doi.org/10.13039/501100000289Breast Cancer Now https://doi.org/10.13039/10000979
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