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1. |
Record Nr. |
UNINA9910798750103321 |
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Titolo |
Essex : the cultural impact of an Elizabethan courtier / / edited by Annaliese Connolly and Lisa Hopkins |
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Pubbl/distr/stampa |
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Manchester, [England] ; ; New York : , : Manchester University Press, , 2014 |
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New York, New York : , : Palgrave Macmillan, , [date of distribution not identified] |
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©2014 |
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ISBN |
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Descrizione fisica |
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1 online resource (337 p.) |
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Disciplina |
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Soggetti |
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Favorites, Royal - England |
LITERARY CRITICISM / Renaissance |
Great Britain Court and courtiers History 16th century |
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Lingua di pubblicazione |
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Formato |
Materiale a stampa |
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Livello bibliografico |
Monografia |
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Note generali |
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Description based upon print version of record. |
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Nota di bibliografia |
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Includes bibliographical references and index. |
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Nota di contenuto |
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ESSEK: The cultural impact of an Elizabethan courtier; Half Title Page; Title Page; Copyright Page; Contents; List of illustrations; Acknowledgements; Notes on contributors; Introduction: Annaliese Connolly and Lisa Hopkins; Part I: Essex: patron and patronage; 1. 'Cleverly playing the stoic': the Earl of Essex, Sir Philip Sidney and surviving Elizabeth's court: Richard Wood; 2. Essexianism and the work of Gervase Markham: Matthew Steggle; 3. Robert Devereux, 2nd Earl of Essex, and the practice of theatre: Grace Ioppolo |
4. Essex's international agenda in 1595 and his device of the Indian Prince: Linda ShenkPart II: Self-fashioning; 5. 'Achilles alter': the heroic lives and afterlives of Robert Devereux, 2nd Earl of Essex: Andrew Hiscock; 6. 'Bringing rebellion broached on his sword': Essex and Ireland: Chris Butler and Willy Maley; 7. Essex's last campaign: the fall of the Earl of Essex and manuscript circulation: Andrew Gordon; Illustrations; 8. 'Idle papers': An Apology of the Earl of Essex: Hugh Gazzard; 9. 'Toucht with bolt of Treason': the Earl of Essex and Lady Penelope Rich: Chris Laoutaris |
10. The Earl of Essex and 'politic history': Alexandra GajdaPart III: |
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Afterlives; 11. Prodigality and the Earl of Essex: Mary Partridge; 12. The Earl of Essex and the Duke of Windsor: Elizabeth and Essex on film: Essex on film; Select bibliography; Index |
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Sommario/riassunto |
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Collection of new essays about the earl of Essex, one of the most important figures of the Elizabethan court |
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2. |
Record Nr. |
UNINA9910227350203321 |
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Autore |
Amadou K. S. Camara |
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Titolo |
Mitochondria: Hubs of Cellular Signaling, Energetics and Redox Balance |
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Pubbl/distr/stampa |
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Descrizione fisica |
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1 online resource (228 p.) |
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Collana |
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Frontiers Research Topics |
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Lingua di pubblicazione |
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Formato |
Materiale a stampa |
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Livello bibliografico |
Monografia |
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Sommario/riassunto |
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Poised at the convergence of most catabolic and anabolic pathways, mitochondria are the center of heterotrophic aerobic life, representing a hub in the overall metabolic network of cells. The energetic functions performed by mitochondria face the unavoidable redox hurdle of handling huge amounts of oxygen while keeping its own as well as the cellular redox environment under control. Reactive oxygen species (ROS) are produced in the respiratory chain as a result of the energy supplying function of mitochondria. Originally considered an unavoidable by-product of oxidative phosphorylation, ROS have become crucial signaling molecules when their levels are kept within physiological range. This occurs when their production and scavenging are balanced within mitochondria and cells. Mitochondria-generated hydrogen peroxide can act as a signaling molecule within mitochondria or in the cytoplasm, affecting multiple networks that control, for example, cell cycle, stress response, cell migration and adhesion, energy metabolism, redox balance, cell contraction, and ion channels. |
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However, under pathophysiological conditions, excessive ROS levels can happen due to either overproduction, overwhelming of antioxidant defenses, or both. Under oxidative stress, detrimental effects of ROS include oxidation of protein, lipids, and nucleic acids; mitochondrial depolarization and calcium overload; and cell-wide oscillations mediated by ROS-induced ROS release mechanisms. Mitochondrial dysfunction is central in the pathogenesis of numerous human maladies including cardiomyopathies and neurodegeneration. Diseases characterized by altered nutrient metabolism, such as diabetes and cancer, exhibit elevated ROS levels. These may contribute to pathogenesis by increasing DNA mutation, affecting regulatory signaling and transcription, and promoting inflammation. Under metabolic stress, several ionic channels present in the inner and outer mitochondrial membranes can have pro-life and -death effects. In the present E-book, based on the Frontiers Research Topic entitled: "Mitochondria: Hubs of cellular signaling, energetics and redox balance", we address one of the fundamental questions that the field of ROS biology faces today: how do mitochondria accomplish a reliable energy provision and at the same time keep ROS levels within physiological, non-harming, limits but crucial for cellular signaling function? Additionally, and within the perspective of mitochondria as signaling-energetic hubs in the extensive cellular metabolic network, we ask how can their collective dynamics scale from the subcellular to the cellular, tissue and organ levels to affect function in health and disease. |
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