Tradurre il fantastico. Dinamiche, strategie, rappresentazioni

Il numero speciale di Lingue e Linguaggi, dal titolo Tradurre il fantastico. Dinamiche, strategie, rappresentazioni offre un contributo al dibattito critico sulla traduzione della letteratura fantastica. Esplorando i peculiari aspetti linguistici, culturali ed editoriali della fantasy in traduzione, i saggi raccolti indagano l’influenza dell’uso di specifiche strategie traduttive sulla sua posizione all’interno del polisistema letterario di arrivo, sulle dinamiche di ricezione e sulla determinazione del suo status all’interno del canone

Tradurre il fantastico. Dinamiche, strategie, rappresentazioni

La traduzione della narrativa fantastica, da intendersi qui nella sua accezione più ristretta e attuale incarnata dalla fantasy e da generi affini, implica una serie articolata di considerazioni traduttologiche che non riguardano solo aspetti linguistici e stilistici, ma chiama in causa fattori di più ampio respiro, come le dinamiche editoriali, la posizione del testo tradotto all’interno del canone e del polisistema di arrivo, gli orizzonti di attesa del lettore, il rapporto tra letteratura e altri media. La rappresentazione di mondi immaginari, a cavallo tra schematicità e creatività, impone ai traduttori una riformulazione di realtà sprovviste di referenti al di fuori del testo e di confrontarsi con una resa dell’alterità che nella fantasy assume contorni ontologicamente definiti, in quanto assoluta e programmatica. A impattare sulla traduzione è anche l’ambiguo status ontologico della letteratura fantastica, non più considerata come genere esclusivamente di consumo, ma neppure del tutto sdoganata come letteratura tout court. Gli effetti sono visibili sul piano delle strategie di resa, che incorrono spesso in un maggiore addomesticamento, naturalizzazione, infantilizzazione delle traduzioni, o nella modifica dei titoli delle opere e nella loro presentazione secondo una certa idea preconcetta delle supposte aspettative del lettore. Ulteriori fattori connessi alla natura del fantastico condizionano la sua dimensione editoriale e le dinamiche di ricezione (serializzazione, affezione, fidelizzazione e transmedialità), agendo anche sull’aspetto traduttivo e aggiungendo ulteriori livelli di complessità. I contributi presenti in questo numero hanno l’obiettivo di rispondere almeno in parte alle questioni fin qui sollevate, col fine ultimo di stimolare un dibattito e un approfondimento che, in ambito traduttologico, risulta ancora carente

HACD1, a regulator of membrane composition and fluidity, promotes myoblast fusion and skeletal muscle growth

The reduced diameter of skeletal myofibres is a hallmark of several congenital myopathies, yet the underlying cellular and molecular mechanisms remain elusive. In this study, we investigate the role of HACD1/PTPLA, which is involved in the elongation of the very long chain fatty acids, in muscle fibre formation. In humans and dogs, HACD1 deficiency leads to a congenital myopathy with fibre size disproportion associated with a generalized muscle weakness. Through analysis of HACD1-deficient Labradors, Hacd1-knockout mice, and Hacd1-deficient myoblasts, we provide evidence that HACD1 promotes myoblast fusion during muscle development and regeneration. We further demonstrate that in normal differentiating myoblasts, expression of the catalytically active HACD1 isoform, which is encoded by a muscle-enriched splice variant, yields decreased lysophosphatidylcholine content, a potent inhibitor of myoblast fusion, and increased concentrations of ≥C18 and monounsaturated fatty acids of phospholipids. These lipid modifications correlate with a reduction in plasma membrane rigidity. In conclusion, we propose that fusion impairment constitutes a novel, non-exclusive pathological mechanism operating in congenital myopathies and reveal that HACD1 is a key regulator of a lipid-dependent muscle fibre growth mechanism

Pazopanib and trametinib as a synergistic strategy against osteosarcoma: Preclinical activity and molecular insights

Receptor tyrosine kinases (RTKs) inhibitors’ activity in advanced osteosarcoma is significant but short-lived. To prevent or at least delay drug resistance, we explored a vertical inhibition by combining drugs acting at different levels of the RTK pathways (pazopanib + trametinib). We studied pazopanib + trametinib antitumor activity both in vitro and in vivo (MNNG-HOS and KHOS xenografts in NOD/SCID mice) investigating the molecular mechanisms and potential escapes. The involvement of MAPK-PI3K pathways was validated by Nanostring technology, western blot and by silencing/overexpression experiments. Pazopanib targets were expressed on seven osteosarcoma cell lines and their pathways were activated. Pazopanib + trametinib exhibited synergistic antitumor activity by inducing apoptosis and inhibiting ERK1/2 and Akt. In vivo antitumor activity was shown in osteosarcoma-bearing mice. The drug combination significantly down-modulated RTK Ephrin Type-A Receptor 2 (EphA2) and Interleukin-7 Receptor (IL-7R), whereas induced mitogen-activated protein-kinase kinase (MAPKK) MEK6. EphA2 silencing significantly reduced osteosarcoma cell proliferation and migration, while impeding MEK6 up-regulation in the treated cells significantly increased the antitumor effect of the studied drugs. Moreover, the up-regulation of MEK6 reduced combination activity. Pazopanib + trametinib demonstrated synergistic antitumor effects in osteosarcoma models through ERK and Akt inhibition and EphA2 and IL-7R down-modulation. MEK6 up-regulation might evoke escaping mechanism

Publisher Correction: Necroptosis Mediates Myofibre Death in Dystrophin-deficient Mice

The original version of this article contained an error in Fig. 3. In panel c, the labels 'mdx' and 'mdx Ripk3-/-' were inadvertently inverted. This has now been corrected in the PDF and HTML versions of the Article

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery