756 research outputs found

    Grace Wyndham Goldie at the BBC: Reappraising the ‘first lady of television’

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    From Crossref journal articles via Jisc Publications RouterMary Irwin - ORCID: 0000-0003-0587-384X https://orcid.org/0000-0003-0587-384XThis working paper explores the significance of the work of the assistant head of BBC Television Talks and Features, Grace Wyndham Goldie, in the development of current affairs and documentary television which took place at the BBC in the late 1950s and early 1960s. Wyndham Goldie was central to these processes. She was passionately committed to the creation of a ‘neutral’ current affairs television, built upon the veracity of the live image. This same passion was not evident in her attitude to the production of documentary television, and she disdained the carefully crafted process of documentary filmmaking. Notably, while Wyndham Goldie was one of a very few women to reach the top of the BBC management ladder, she offered limited encouragement and support to other women working at the corporation.pubpu

    The process of reclassification in the public service of the Commonwealth of Massachusetts

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    Thesis (M.A.)--Boston Univesity, 1944. This item was digitized by the Internet Archive

    Leakage-Aware Interconnect for On-Chip Network

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    On-chip networks have been proposed as the interconnect fabric for future systems-on-chip and multi-processors on chip. Power is one of the main constraints of these systems and interconnect consumes a significant portion of the power budget. In this paper, we propose four leakage-aware interconnect schemes. Our schemes achieve 10.13%~63.57% active leakage savings and 12.35%~95.96% standby leakage savings across schemes while the delay penalty ranges from 0% to 4.69%.Comment: Submitted on behalf of EDAA (http://www.edaa.com/

    A Role For Lipid Rafts In Egfr Tki Resistance In Breast Cancer

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    Breast cancer can be divided into genetic sub-types including luminal, HER2+, and basal-type. With the introduction of targeted therapies against estrogen receptor and HER2 receptor mortality rates of American women with breast cancer have declined. Unfortunately, basal-type breast cancers, which have the worst clinical outcome, do not express estrogen receptor or HER2, and as such, have no targeted therapeutic option. The epidermal growth factor receptor is an attractive target for therapeutics in basal-type breast cancer, as it is over-expressed in 60% of these cases. Also, over-expression of EGFR correlates with poor patient prognosis. Unfortunately, inhibitors of EGFR have shown little clinical efficacy in basal-type breast cancers. We have utilized basal-type breast cancer cell lines to determine a potential mechanism of resistance to EGFR-targeted small molecule tyrosine kinase inhibitors (TKIs). Specifically, we have shown that EGFR localizes to discrete membrane microdomains (lipid rafts) in cell lines that are resistant to EGFR TKI-induced growth inhibition. Depletion of lipid rafts via cholesterol reduction results in sensitivity of EGFR TKI resistant breast cancer cell lines to the EGFR TKI gefitinib. Importantly, the effects of cholesterol lowering drugs and EGFR TKI in combination were synergistic. We have shown that the non-receptor tyrosine kinase c-Src, which is co-over-expressed with EGFR in a subset of breast tumors, also localizes to lipid rafts in the SUM159 breast cancer cell line. In this model system, c-Src kinase inhibition results in synergistically decreased cell viability in combination with EGFR tyrosine kinase inhibition. c-Src kinase inhibition and cholesterol depletion are additive, results that suggest these two inhibitors work within the same pathway. Indeed, treatment with either cholesterol lowering drugs or c-Src kinase inhibitors results in decreased EGFR-kinase independent Akt phosphorylation. Thus, lipid rafts may provide a platform whereby EGFR and c-Src interact to promote Akt signaling in the absence of EGFR kinase activity. These results suggest, for the first time, that lipid rafts are involved in EGFR-kinase independent signaling, and that depletion of these rafts may work in combination with EGFR tyrosine kinase inhibition to decrease breast cancer cell growth

    A Performance Comparison of a Technical Trading System with ARIMA and VAR Models for Soybean Complex Prices

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    Both technical trading systems and standard economic time series models are based upon the assumption that current market prices are not independent of past market behavior. This study examines the relative performance of a Channel (CHL) technical trading system with an Autoregressive Integrated Moving Average (ARIMA) model and a Vector Autoregressive (VAR) model in forecasting soybean, soybean meal, and soybean oil prices over the period January 1984-June 1988. ARIMA and VAR models are developed over the time period January 1974-December 1983 and then are used to forecast out-of-sample from January 1984 through June 1988. The CHL trading signals and out-of-sample two month ahead forecasts from the ARIMA and VAR models are used to take positions in the futures markets. The resulting trading returns are evaluated to determine the relative economic performance of the models within the soybean complex. Of these models, the CHL technical trading system exhibits consistent trading returns across the soybean complex. Furthermore, the CHL technical trading system is robust across the two subperiods of the out-of-sample period, one of which is characterized by rising commodity prices and the other by declining commodity prices. These results suggest that in the short run, regularities within a single price series can be used to forecast prices within the soybean complex. Further, technical trading system prove more useful in utilizing such regularities for forecasting than the autoregressive or moving average processes found in either ARIMA or VAR modeling techniques

    Targeting Nucleotide Biosynthesis: A Strategy for Improving the Oncolytic Potential of DNA Viruses

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    The rapid growth of tumors depends upon elevated levels of dNTPs, and while dNTP concentrations are tightly regulated in normal cells, this control is often lost in transformed cells. This feature of cancer cells has been used to advantage to develop oncolytic DNA viruses. DNA viruses employ many different mechanisms to increase dNTP levels in infected cells, because the low concentration of dNTPs found in non-cycling cells can inhibit virus replication. By disrupting the virus-encoded gene(s) that normally promote dNTP biosynthesis, one can assemble oncolytic versions of these agents that replicate selectively in cancer cells. This review covers the pathways involved in dNTP production, how they are dysregulated in cancer cells, and the various approaches that have been used to exploit this biology to improve the tumor specificity of oncolytic viruses. In particular, we compare and contrast the ways that the different types of oncolytic virus candidates can directly modulate these processes. We limit our review to the large DNA viruses that naturally encode homologs of the cellular enzymes that catalyze dNTP biogenesis. Lastly, we consider how this knowledge might guide future development of oncolytic viruses
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