19 resultados para Stewart, Alexander Turney, 1802-1876.


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A second English translation of Alexander von Humboldt's account of travel to South America, the Relation historique (1814–25), was published between 1852 and 1853. Appearing some 30 years after the first seven-volume translation (1814–29) by Helen Maria Williams, this second rendering of the Personal Narrative by Thomasina Ross was an abridged version that aimed to make Humboldt's travelogue more relevant to the mid-century reader. This translation has largely been overlooked by Humboldt scholars, despite it being a far more affordable, accessible and popular edition. I discuss here how Ross's revisions can be understood within a larger process of rereading and revision that responded to critics’ assessments of the first translation. Emphasising the status of the Personal Narrative as a text in flux, I assess how Ross modernised it to meet the demands of a new readership, recasting the image that Humboldt had constructed of himself as a travelling scientist, scientific writer and member of the international scientific community.

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A study of the use of hybrid physical appearance both to signal and to explore the disputed paternity of Alexander the Great throughout its vernacular French tradition. The article compares the 'child of Babylon' portent and Alexander's son Alior in the twelfth-century French "Roman d'Alexandre" poem cycle, and a fifteenth-century prose adaptation of it.

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This article examines a 14th-c. translation into Old Occitan prose of a late-antique life of Alexander the Great: Justin’s Epitome of the 'Historia Philippicae' of Pompeius Trogus. The article argues that it is the work of translators whose knowledge of pagan Latin materials was incomplete and whose use of their native tongue rested on non-literary bases. This text has not been edited before, and examining its uneven treatment of its source provides important new insights into the work of translators in the later Middle Ages. In conclusion, the article suggests some new approaches to the understanding of translation as a process of reconstruction and adaptation.

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Therapeutic activation of Toll-like receptors (TLR) has potential for cancer immunotherapy, for augmenting the activity of anti-tumor monoclonal antibodies (mAbs), and for improved vaccine adjuvants. A previous attempt to specifically target TLR agonists to dendritic cells (DC) using mAbs failed because conjugation led to non-specific binding and mAbs lost specificity. We demonstrate here for the first time the successful conjugation of a small molecule TLR7 agonist to an anti-tumour mAb (the anti-hCD 20 rituximab) without compromising antigen specificity. The TLR7 agonist UC-1V150 was conjugated to rituximab using two conjugation methods and yield, molecular substitution ratio, retention of TLR7 activity and specificity of antigen binding were compared. Both conjugation methods produced rituximab-UC-1V150 conjugates with UC-1V150 : rituximab ratio ranging from 1:1 to 3:1 with drug loading quantified by UV spectroscopy and drug substitution ratio verified by MALDI TOF mass spectroscopy. The yield of purified conjugates varied with conjugation method, and dropped as low as 31% using a method previously described for conjugating UC-1V150 to proteins, where a bifunctional crosslinker was firstly reacted with rituximab, and secondly to the TLR7 agonist. We therefore developed a direct conjugation method by producing an amine-reactive UV active version of UC-1V150, termed NHS:UC-1V150. Direct conjugation with NHS:UC-1V150 was quick and simple and gave improved conjugate yields of 65-78%. Rituximab-UC-1V150 conjugates had the expected pro-inflammatory activity in vitro (EC50 28-53 nM) with a significantly increased activity over unconjugated UC-1V150 (EC50 547 nM). Antigen binding and specificity of the rituxuimab-UC-1V150 conjugates was retained, and after incubation with human peripheral blood leukocytes, all conjugates bound strongly only to CD20-expressing B cells whilst no non-specific binding to CD20-negative cells was observed. Selective targeting of Toll-like receptor activation directly within tumors or to DC is now feasible.