23 research outputs found

    Damaged Type and Areopagitica's Clandestine Printers

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    Milton’s Areopagitica (1644) is one of the most significant texts in the history of the freedom of the press, and yet the pamphlet’s clandestine printers have successfully eluded identification for over 375 years. By examining distinctive and dam-aged type pieces from 100 pamphlets from the 1640s, this article attributes the print-ing of Milton’s Areopagitica to the London printers Matthew Simmons and Thomas Paine, with the possible involvement of Gregory Dexter. It further reveals a sophisti-cated ideological program of clandestine printing executed collaboratively by Paine and Simmons throughout 1644 and 1645 that includes not only Milton’s Areopagitica but also Roger Williams’s The Bloudy Tenent of Persecution, William Walwyn’s The Compassionate Samaritane, Henry Robinson’s Liberty of Conscience, Robinson’s John the Baptist, and Milton’s Of Education, Tetrachordon, and Colasterion

    Canst Thou Draw Out Leviathan with Computational Bibliography? New Angles on Printing Thomas Hobbes’ “Ornaments” Edition

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    This article attributes one of the three “first” editions of Leviathan to the London printer John Richardson (fl. 1673–1703), revising Noel Malcolm’s attribution to a different printer in the recent Clarendon Edition of Leviathan. We lay out the mystery of Leviathan’s so-called “Ornaments” edition and use evidence from damaged type pieces to say why we attribute its printing to Richardson. We then give a short sketch of Richardson’s life and career and present evidence that supports a new date for the edition, including newly discovered advertisements and evidence from deteriorating type. We conclude with some implications for book history and bibliography, on the one hand, and Hobbes scholarship on the other. We argue that what we call “computational bibliography”—the analysis of bibliographical evidence through computational methods such as machine learning and computer vision— offers new angles for seeing the materiality and craft of clandestine, anonymously-printed books like Hobbes’ Leviathan

    Who Rpinted Shakespeare’s Fourth Folio?

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    According to Fredson Bowers, writing in Shakespeare Quarterly in 1951, we will never know the printer of that section "until we know everything there is to be learned about seventeenth-century types." 2 Bowers doubted we could ever list the full set of F4's printers because F4 was printed anonymously, and the volume left few clues about its printers. While George Watson Cole's 1909 "examination of the letterpress show[ed] that a copy of the Third Folio was apparently broken into three portions and sent to three different printers," Bowers himself only got as far as attributing the first of F4's three separately paginated parts. 3 The purpose of this note is to identify the other two printers involved in F4, one of whom, John Macock, was the printer whose shop was responsible for F4's Hamlet. Regrettably, this short note does not include everything there is to be learned about seventeenth-century types.

    Hydrogen Epoch of Reionization Array (HERA)

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    The Hydrogen Epoch of Reionization Array (HERA) is a staged experiment to measure 21 cm emission from the primordial intergalactic medium (IGM) throughout cosmic reionization (z=6−12z=6-12), and to explore earlier epochs of our Cosmic Dawn (z∌30z\sim30). During these epochs, early stars and black holes heated and ionized the IGM, introducing fluctuations in 21 cm emission. HERA is designed to characterize the evolution of the 21 cm power spectrum to constrain the timing and morphology of reionization, the properties of the first galaxies, the evolution of large-scale structure, and the early sources of heating. The full HERA instrument will be a 350-element interferometer in South Africa consisting of 14-m parabolic dishes observing from 50 to 250 MHz. Currently, 19 dishes have been deployed on site and the next 18 are under construction. HERA has been designated as an SKA Precursor instrument. In this paper, we summarize HERA's scientific context and provide forecasts for its key science results. After reviewing the current state of the art in foreground mitigation, we use the delay-spectrum technique to motivate high-level performance requirements for the HERA instrument. Next, we present the HERA instrument design, along with the subsystem specifications that ensure that HERA meets its performance requirements. Finally, we summarize the schedule and status of the project. We conclude by suggesting that, given the realities of foreground contamination, current-generation 21 cm instruments are approaching their sensitivity limits. HERA is designed to bring both the sensitivity and the precision to deliver its primary science on the basis of proven foreground filtering techniques, while developing new subtraction techniques to unlock new capabilities. The result will be a major step toward realizing the widely recognized scientific potential of 21 cm cosmology.Comment: 26 pages, 24 figures, 2 table

    Genetic mechanisms of critical illness in COVID-19.

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    Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

    Transforming growth factors (TGFα and TGFÎČH) stimulate chondroitin sulfate and hyaluronate synthesis in cultured rat liver fat storing cells

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    AbstractThe synthesis of total sulfated glycosaminoglycans (GAG) was stimulated by transforming growth factors (TGFα 1.4-fold at 5 ngml, and TGFÎČ1 2.05-fold at 2.5 ngml) in primary cultures of rat liver fat storing cells (FSC). The combination of both TGFs resulted in an additively stimulated synthesis of total sulfated GAG (more than 3-fold), chondroitin sulfate (more than 15-fold) and hyaluronate (3.8-fold), respectively, whereas the formation of dermatan sulfate was unchanged and that of heparan sulfate was slightly reduced. In summary, TGFs were identified as important mediators of stimulated GAG synthesis in those cells of the liver (FSC), which are the primary site of matrix glycoconjugate production.Fat storing cell; Fibrogenesis; Glycosaminoglycans; Chondroitin sulfate; Hyaluronic acid; Transforming growth facto
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