Una poeta: Perspectives on the Translation of Janet Frame’s Verse into Italian

ABSTRACT Janet Frame (1924–2004) is known for being one of the most prolific, translated, and unconventional New Zealand novelists. Her work, however, includes a vast production of poems, which scholars and translators have ignored or, at least, not considered worthy for a comprehensive approach to her. Frame’s work has undergone the further limitation of a strongly biography-based hermeneutics: from the gossiping around her alleged schizophrenia, to the popularity of the filmic version of her autobiography (An Angel at My Table) by Jane Campion, and the countless legends that have sprung around her, she has often been stigmatised and labelled the ‘mad writer’ of Campion’s movie. This thesis links the risks of the life/myth-driven perspectives to the current lack of interest in Frame’s poetry. Her poetic production is here presented as a fundamental part of her oeuvre and her idiosyncratic approach to writing. Therefore, this study aims to fill this gap in the literature on Frame and thus reconfigure her role as a poet. Through a combination of methodologies grounded in literary and verse translation theories, creativity and genre studies, poststructuralism and postcolonialism, this thesis investigates the most significant traits of Frame’s prose and poetry, particularly the traits shared by both. It critiques past translations of Frame’s prose into Italian where these have not taken into account the poetic value of her work, and suggests strategies for the translation of her verse into Italian, arguing that an informed approach to her poetry in translation may greatly contribute to a reconfiguration and re-evaluation of her legacy

Metabolic underpinnings of the paradoxical net phosphocreatine resynthesis in contracting rat gastrocnemius muscle

AbstractNet phosphocreatine (PCr) resynthesis during muscle contraction is a paradoxical phenomenon because it occurs under conditions of high energy demand. The metabolic underpinnings of this phenomenon were analyzed non-invasively using 31P-magnetic resonance spectroscopy in rat gastrocnemius muscle (n=11) electrically stimulated (7.6 Hz, 6 min duration) in situ under ischemic and normoxic conditions. During ischemic stimulation, [PCr] initially fell to a steady state (9±5% of resting concentration) which was maintained for the last 5 min of stimulation, whereas isometric force production decreased to a non-measurable level beyond 3 min. Throughout normoxic stimulation, [PCr] and force production declined to a steady state after respectively 1 min (5±3% of resting concentration) and 3.25 min (21±8% of initial value) of stimulation. Contrary to the observations under ischemia, a paradoxical net PCr resynthesis was recorded during the last 2 min of normoxic stimulation and was not accompanied by any improvement in force production. These results demonstrate that the paradoxical net PCr resynthesis recorded in contracting muscle relies exclusively on oxidative energy production and could occur in inactivated fibers, similarly to PCr resynthesis during post-exercise recovery

31P Magnetic resonance spectroscopy study of phosphocreatine recovery kinetics in skeletal muscle: the issue of intersubject variability

AbstractWe have analyzed by 31P MRS the relationship between kinetic parameters of phosphocreatine (PCr) recovery and end-of-exercise status under conditions of moderate and large acidosis induced by dynamic exercise. Thirteen healthy subjects performed muscular contractions at 0.47 Hz (low frequency, moderate exercise) and 0.85 Hz (high frequency, heavy exercise). The rate constant of PCr resynthesis (kPCr) varied greatly among subjects (variation coefficients: 43 vs. 57% for LF vs. HF exercises) and protocols (kPCr values: 1.3±0.5 min−1 vs. 0.9±0.5 min−1 for LF vs. HF exercises, P<0.03). The large intersubject variability can be captured into a linear relationship between kPCr, the amount of PCr consumed ([PCr2]) and pH reached at the end of exercise (pHend) (kPCr=−3.3+0.7 pHend-0.03 [PCr2]; P=0.0007; r=0.61). This dual relationship illustrates that mitochondrial activity is affected by end-of-exercise metabolic status and allows reliable comparisons between control, diseased and trained muscles. In contrast to kPCr, the initial rate of PCr recovery and the maximum oxidative capacity were always constant whatever the metabolic conditions of end-of-exercise and can then be additionally used in the identification of dysfunctions in the oxidative metabolic pathway

EmbR2, a structural homologue of EmbR, inhibits the Mycobacterium tuberculosis kinase/substrate pair PknH/EmbR

International audienceEmbR is a transcriptional regulator that is phosphorylated by the cognate mycobacterial STPK (serine/threonine protein kinase) PknH. Recent studies demonstrated that PknH-dependent phosphorylation of EmbR enhances its DNA-binding activity and activates the transcription of the embCAB genes encoding arabinosyltransferases, which participate in arabinan biosynthesis. In the present study, we identified a genomic region of 4425 bp, which is present in Mycobacterium tuberculosis CDC1551, but absent from M. tuberculosis H37Rv, comprising the MT3428 gene, which is homologous with embR. Homology modelling of the MT3428 gene product illustrated its close relationship (56% identity) to EmbR, and it was hence termed EmbR2. In marked contrast with EmbR, EmbR2 was not phosphorylated by PknH, although it is a substrate of other M. tuberculosis kinases, including PknE and PknF. Tryptophan fluorescence emission of EmbR2 was monitored in the presence of three different PknH-derived phosphopeptides and demonstrated that EmbR2 binds to at least two of the threonine sites known to undergo autophosphorylation in PknH. We observed that the capacity of EmbR2 to interact physically with PknH without being phosphorylated was a result of EmbR2-mediated inhibition of kinase activity: incubation of PknH with increasing concentrations of EmbR2 led to a dose-response inhibition of the autokinase activity, similarly to O6-cyclohexylmethylguanine, a known inhibitor of eukaryotic cyclin-dependent kinases. Moreover, EmbR2 inhibited PknH-dependent phosphorylation of EmbR in a dose-dependent manner. Together, these results suggest that EmbR2 is a regulator of PknH activation, thus directly participating in the control of the PknH/EmbR pair and potentially in mycobacterial physiology/virulence of M. tuberculosis CDC1551

Deletion of TRAAK Potassium Channel Affects Brain Metabolism and Protects against Ischemia

Cerebral stroke is a worldwide leading cause of disability. The two-pore domain K(+) channels identified as background channels are involved in many functions in brain under physiological and pathological conditions. We addressed the hypothesis that TRAAK, a mechano-gated and lipid-sensitive two-pore domain K(+) channel, is involved in the pathophysiology of brain ischemia. We studied the effects of TRAAK deletion on brain morphology and metabolism under physiological conditions, and during temporary focal cerebral ischemia in Traak(-/-) mice using a combination of in vivo magnetic resonance imaging (MRI) techniques and multinuclear magnetic resonance spectroscopy (MRS) methods. We provide the first in vivo evidence establishing a link between TRAAK and neurometabolism. Under physiological conditions, Traak(-/-) mice showed a particular metabolic phenotype characterized by higher levels of taurine and myo-inositol than Traak(+/+) mice. Upon ischemia, Traak(-/-) mice had a smaller infarcted volume, with lower contribution of cellular edema than Traak(+/+) mice. Moreover, brain microcirculation was less damaged, and brain metabolism and pH were preserved. Our results show that expression of TRAAK strongly influences tissue levels of organic osmolytes. Traak(-/-) mice resilience to cellular edema under ischemia appears related to their physiologically high levels of myo-inositol and of taurine, an aminoacid involved in the modulation of mitochondrial activity and cell death. The beneficial effects of TRAAK deletion designate this channel as a promising pharmacological target for the treatment against stroke

P-31 Magnetic Resonance Spectroscopy. A tool for diagnostic purposes and pathophysiological insights in muscle diseases

It has been more than 15 years since 31-phosphorus magnetic resonance spectroscopy (31P-MRS) was first used in order to study human muscle diseases. Its impact on the field of neuromuscular disorders has now become considerable for pathophysiological insights and for diagnostic purposes. Recent reviews (1-3) have summarized the possibilities of the technique that permits to investigate muscle energetic metabolism non-invasively and non-destructively. In this mini-review, we will recall the information provided by a P-31 MRS spectrum when exploring a normal muscle and present the new spectral semiology that is helpful for the diagnosis of metabolic myopathies. We will also show briefly some other clinical applications of this technique

Induction of Human Immunodeficiency Virus (HIV-1) Envelope Specific Cell-Mediated Immunity by a Non-Homologous Synthetic Peptide

Peer reviewed: YesNRC publication: Ye