135 resultados para Lever, Charles James, 1806-1872.
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Accepted for publication - will appear in advance view JEL and hard copy publication in (2012) Vol 24(2).
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This article explores the significance of the adopted partial pseudonym “Clarence” to James Clarence Mangan (1803-1849), who is increasingly regarded as the most important Irish poet before W. B. Yeats. Tracing the literary history of “Clarence” from Shakespeare to Maria Edgeworth, this essay argues that the intriguing adoption exposes a preoccupation with themes of unlawful textual copying that is at the centre of Mangan’s imagination. These tropes assume singular significance when appreciated alongside Mangan’s profession as a scrivener. While literary criticism has separated Mangan the poet from Mangan the legal scribe, his hitherto under-explored assumption of “Clarence” provides a clue to their close and crucial connection. These themes of pseudonymity, copying, and criminality combine with particular resonance in his quasi-translation “The Man in the Cloak” (1838) to open up new perspectives on Mangan’s writing and its participation in wider European cultural contexts and concerns. The essay will conclude with a salient comparison of Mangan’s story with Nikolay Gogol’s seminal story “The Overcoat”, or, “The Cloak” (1842).
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Objective: Pharmacological profiling of store-operated Ca(2+) entry (SOCE) and molecular profiling of ORAI and TRPC expression in arterioles.
Methods: Fura-2 based microfluorimetry was used to assess CPA-induced SOCE in rat retinal arteriolar myocytes. Arteriolar ORAI and TRP transcript expression were screened using RT-PCR.
Results: SKF96365 and LOE908 blocked SOCE (IC(50) s of 1.2µM and 1.4µM, respectively). Gd(3+) and La(3+) potently inhibited SOCE (IC(50) s of 21nM and 42nM, respectively), but Ni(2+) showed lower potency (IC(50) = 11.6µM). 2-aminoethyldiphenyl borate (2APB) inhibited SOCE (IC(50) = 3.7µM) but enhanced basal influx (>100µM). Verapamil and nifedipine had no effect at concentrations that inhibit L-type Ca(2+) channels, but diltiazem inhibited SOCE by approximately 40% (=0.1µM). RT-PCR demonstrated transcript expression for ORAI 1, 2 and 3, and TRPC1, 3, 4 and 7. Transcripts for TRPV1 and 2, which are activated by 2APB, were also expressed.
Conclusion: The pharmacological profile of SOCE in retinal arteriolar smooth muscle appears unique when compared to other vascular tissues. This suggests that the molecular mechanisms underlying SOCE can differ, even in closely related tissues. Taken together, the pharmacological and molecular data are most consistent with involvement of TRPC1 in SOCE, although involvement of ORAI or other TRPC channels cannot be excluded. © 2012 John Wiley & Sons Ltd.