Mito, tragedia y metateatro en el teatro espanol del siglo XX : ensayo sobre el cuerpo y la conciencia en el drama

RÉSUMÉMythe, tragédie et méta-théâtre sont des termes techniques provenant de disciplines comme l'anthropologie, l'histoire, la théorie et la critique littéraires. Malgré le fait que l'on puisse les assigner à des périodes historiques déterminées, ce sont des notions qui ont encore un sens à la fois actuel (elles sont indispensables pour comprendre le théâtre contemporain) et concret (à travers les différentes poétiques qui les reconfigurent, elles affectent le spectateur d'une certaine façon, ont un effet déterminé sur son corps et sa conscience). Je propose donc de les définir synthétiquement en fonction de l'effet qu'ils produisent sur le spectateur qui est conçu comme une unité de corps et de conscience. Le corps étant défini comme le lieu des émotions, la conscience sera la connaissance que le sujet acquiert de soi et du monde en fonction de ces émotions. Or, le mûthos génère des émotions que la tragédie purge à travers le phénomène de la catharsis. En revanche, le méta-théâtre interrompt le processus émotif de la conscience. Tout en appuyant mes définitions sur des notions de psychologie, neurologie et physique quantique, j'oppose tragédie et méta-théâtre de la façon suivante: la tragédie produit une forme de conscience incarnée chez le spectateur, alors que le méta-théâtre n'aboutit qu'à une forme de conscience cartésienne ou vision désincarnée. J'applique ensuite cette conception à une série de pièces importantes de l'histoire du théâtre espagnol au XXe siècle qui comportent toutes une part de réécriture d'un ou de plusieurs mythes. Je constate une généralisation du traitement méta-théâtral de la réécriture, au détriment non du tragique, mais de la tragédie proprement dite. Par conséquent, je diagnostique un déficit d'incarnation dans le théâtre espagnol au XXe siècle.

Il viaggio di Faust in Italia : percorsi di ricezione di un mito moderno

La tesi descrive il fenomeno di ricezione del mito faustiano all'interno della tradizione letteraria italiana di Otto e Novecento (1808-1945) nel suo sviluppo diacronico, individuando i nodi processuali emergenti ritenuti sistematici accanto alle tipologie predominanti della risposta testuale e alle più proficue rifunzionalizzazioni letterarie. La storia del mito di Faust è stata considerata aristotelicamente nella sua natura complessa ed evolutiva di fabula rinarrata, e di volta in volta risemantizzata in nuovi sistemi di valori, estetici e ideologici. Ma soprattutto in nuovi sistemi testuali. Scopo primario è stato infatti quello di comprendere come il mito di Faust sia entrato dentro alla cultura letteraria italiana e come abbia agito al suo interno, interferendo con essa. Naturalmente lo scambio e gli sviluppi hanno investito in modo reciproco e la tradizione accogliente e il mito stesso, producendo un allargamento esegetico delle sue possibilità semantiche: è infatti emersa una storia testuale che tematizza nel tempo il medesimo mito lungo assi interpretative anche estremamente divergenti. La ricerca ha portato alla scoperta di una ricca testualità rimossa dal canone della storia della letteratura italiana, anche se spesso prevalgono i testi-documento sui testi esteticamente più validi e significativi in sé; si tratta di una testualità talmente quantitativamente ricca da invitare ad un ripensamento qualitativo del fenomeno generale. Il mito di Faust, per due secoli percepito dalla critica dominante come distante ed estraneo alla cultura letteraria italiana, è invece riuscito ad entrare nella tradizione letteraria italiana, anche se attraverso modalità molto controverse: in linea di massima è potuto passare dal canone statico al canone dinamico laddove ha saputo influenzare e stimolare nuove vie significative di sviluppo formale. Il confronto della cultura letteraria italiana con il mito di Faust è stato in effetti caratterizzato subito da un doppio movimento discratico di rifiuto e dialogo. Il principale fattore di rifiuto è stato di carattere culturale: la difficoltà ad accettare un equilibrio fatto non di antitesi risolte in una sintesi ma di polarità aperte, irrisolte, in perpetuo bilanciamento, anche a livello formale reso in una tragedia franta in scene apparentemente autonome, divisa in due parti così diverse e chiusa da un lieto fine, mal si confaceva ai diffusi canoni classicisti di equilibrio formale, nonché alle esigenze romantiche di poesia moralmente chiara nel suo messaggio. Da qui le diffuse accuse di scarsa chiarezza e ambiguità morale, che andavano direttamente ad incontrarsi e sommarsi con i pregiudizi più propriamente teologico- religiosi di estraneità a quel mito nato come saga luterana dichiaratamente anti-papale. La condanna di carattere moralistico-cattolico risulta nei fatti propria più di certa cultura che non del largo pubblico che invece nel corso dell'Ottocento dimostra di gradire le versioni per musica e balletto di argomento faustiano, per quanto semplificata ed edulcorate rispetto alla leggenda originaria così come rispetto alla tragedia goethiana. Rispetto a tutti questi elementi di resistenza e rifiuto l'opera Mefistofele di Boito si presenta come snodo di opposizione consapevole e riferimento duraturo d'interrogazione critica. La principale linea di avvicinamento invece tra la cultura letteraria italiana e il mito di Faust resta quella del parallelo, già ideato dagli stessi intellettuali tedeschi d'inizio Ottocento, con l'opera ritenuta massima nel nuovo canone nazionale italiano da fine Settecento ad oggi: la Divina Commedia. Tanta critica, almeno fino alla metà del XX secolo, si rifà più o meno esplicitamente a questo parallelo pregiudiziale e testualmente piuttosto infondato ma molto produttivo, come si è attestato, a livello creativo. Questa ricostruzione ha voluto nel suo complesso dimostrare sul campo il valore di questo macrotesto faustiano come una delle vie maestre della dialettica tra tradizione e modernità, ancor più significativa nell'ambito di una cultura letteraria come quella italiana che, dopo l'estinguersi della sua centralità in epoca rinascimentale, si è rivelata particolarmente resistente al dialogo con le altre letterature fino al pieno Novecento.

Skeletal muscle mitochondria in the elderly: effects of physical fitness and exercise training.

CONTEXT: Sarcopenia is thought to be associated with mitochondrial (Mito) loss. It is unclear whether the decrease in Mito content is consequent to aging per se or to decreased physical activity. OBJECTIVES: The objective of the study was to examine the influence of fitness on Mito content and function and to assess whether exercise could improve Mito function in older adults. DESIGN AND SUBJECTS: Three distinct studies were conducted: 1) a cross-sectional observation comparing Mito content and fitness in a large heterogeneous cohort of older adults; 2) a case-control study comparing chronically endurance-trained older adults and sedentary (S) subjects matched for age and gender; and 3) a 4-month exercise intervention in S. SETTING: The study was conducted at a university-based clinical research center. OUTCOMES: Mito volume density (MitoVd) was assessed by electron microscopy from vastus lateralis biopsies, electron transport chain proteins by Western blotting, mRNAs for transcription factors involved in M biogenesis by quantitative RT-PCR, and in vivo oxidative capacity (ATPmax) by (31)P-magnetice resonance spectroscopy. Peak oxygen uptake was measured by graded exercise test. RESULTS: Peak oxygen uptake was strongly correlated with MitoVd in 80 60- to 80-year-old adults. Comparison of chronically endurance-trained older adults vs S revealed differences in MitoVd, ATPmax, and some electron transport chain protein complexes. Finally, exercise intervention confirmed that S subjects are able to recover MitoVd, ATPmax, and specific transcription factors. CONCLUSIONS: These data suggest the following: 1) aging per se is not the primary culprit leading to Mito dysfunction; 2) an aerobic exercise program, even at an older age, can ameliorate the loss in skeletal muscle Mito content and may prevent aging muscle comorbidities; and 3) the improvement of Mito function is all about content.

Mitochondrial reactive oxygen species generation triggers inflammatory response and tissue injury associated with hepatic ischemia-reperfusion: Therapeutic potential of mitochondrially targeted antioxidants.

Mitochondrial reactive oxygen species generation has been implicated in the pathophysiology of ischemia-reperfusion (I/R) injury; however, its exact role and its spatial-temporal relationship with inflammation are elusive. Herein we explore the spatial-temporal relationship of oxidative/nitrative stress and inflammatory response during the course of hepatic I/R and the possible therapeutic potential of mitochondrial-targeted antioxidants, using a mouse model of segmental hepatic ischemia-reperfusion injury. Hepatic I/R was characterized by early (at 2h of reperfusion) mitochondrial injury, decreased complex I activity, increased oxidant generation in the liver or liver mitochondria, and profound hepatocellular injury/dysfunction with acute proinflammatory response (TNF-α, MIP-1α/CCL3, MIP-2/CXCL2) without inflammatory cell infiltration, followed by marked neutrophil infiltration and a more pronounced secondary wave of oxidative/nitrative stress in the liver (starting from 6h of reperfusion and peaking at 24h). Mitochondrially targeted antioxidants, MitoQ or Mito-CP, dose-dependently attenuated I/R-induced liver dysfunction, the early and delayed oxidative and nitrative stress response (HNE/carbonyl adducts, malondialdehyde, 8-OHdG, and 3-nitrotyrosine formation), and mitochondrial and histopathological injury/dysfunction, as well as delayed inflammatory cell infiltration and cell death. Mitochondrially generated oxidants play a central role in triggering the deleterious cascade of events associated with hepatic I/R, which may be targeted by novel antioxidants for therapeutic advantage.

Physiopathologie du coeur embryonnaire soumis à l'anoxie-réoxygénation: rôle protecteur du NO et des canaux KATP

RESUME Introduction : Dans le coeur adulte, l'ischémie et la reperfusion entraînent des perturbations électriques, mécaniques, biochimiques et structurales qui peuvent causer des dommages réversibles ou irréversibles selon la sévérité de l'ischémie. Malgré les récents progrès en cardiologie et en chirurgie foetales, la connaissance des mécanismes impliqués dans la réponse du myocarde embryonnaire à un stress hypoxique transitoire demeure lacunaire. Le but de ce travail a donc été de caractériser les effets chrono-, dromo- et inotropes de l'anoxie et de la réoxygénation sur un modèle de coeur embryonnaire isolé. D'autre part, les effets du monoxyde d'azote (NO) et de la modulation des canaux KATP mitochondriaux (mito KATP) sur la récupération fonctionnelle postanoxique ont été étudiés. La production myocardique de radicaux d'oxygène (ROS) et l'activité de MAP Kinases (ERK et JNK) impliquées dans la signalisation cellulaire ont également été déterminées. Méthodes : Des coeurs d'embryons de poulet âgés de 4 jours battant spontanément ont été placés dans une chambre de culture puis soumis à une anoxie de 30 min suivie d'une réoxygénation de 60 min. L'activité électrique (ECG), les contractions de l'oreillette, du ventricule et du conotroncus (détectées par photométrie), la production de ROS (mesure de la fluorescence du DCFH) et l'activité kinase de ERK et JNK dans le ventricule ont été déterminées au cours de l'anoxie et de la réoxygénation. Les coeurs ont été traités avec un bloqueur des NO synthases (L-NAME), un donneur de NO (DETA-NONOate), un activateur (diazoxide) ou un inhibiteur (5-HD) des canaux mitoKATP un inhibiteur non-spécifique des PKC (chélérythrine) ou un piégeur de ROS (MPG). Résultats : L'anoxie et la réoxygénation entraînaient des arythmies (essentiellement d'origine auriculaire) semblables à celles observées chez l'adulte, des troubles de la conduction (blocs auriculo-ventriculaires de 1er, 2ème et 3ème degré) et un ralentissement marqué du couplage excitation-contraction (E-C) ventriculaire. En plus de ces arythmies, la réoxygénation déclenchait le phénomène de Wenckelbach, de rares échappements ventriculaires et une sidération myocardique. Aucune fibrillation, conduction rétrograde ou activité ectopique n'ont été observées. Le NO exogène améliorait la récupération postanoxique du couplage E-C ventriculaire alors que L'inhibition des NOS la ralentissait. L'activation des canaux mito KATP augmentait la production mitochondriale de ROS à la réoxygénation et accélérait la récupération de la conduction (intervalle PR) et du couplage E-C ventriculaire. La protection de ce couplage était abolie par le MPG, la chélérythrine ou le L-NAME. Les fonctions électrique et contractile de tous les coeurs récupéraient après 30-40 min de réoxygénation. L'activité de ERK et de JNK n'était pas modifiée par L'anoxie, mais doublait et quadruplait, respectivement, après 30 min de réoxygénation. Seule l'activité de JNK était diminuée (-60%) par l'activation des canaux mitoKATP. Cet effet inhibiteur était partiellement abolit par le 5-HD. Conclusion: Dans le coeur immature, le couplage E-C ventriculaire semble être un paramètre particulièrement sensible aux conditions d'oxygénation. Sa récupération postanoxique est améliorée par l'ouverture des canaux mitoKATP via une signalisation impliquant les ROS Ies PKC et le NO. Une réduction de l'activité de JNK semble également participer à cette protection. Nos résultats suggèrent que les mitochondries jouent un rôle central dans la modulation des voies de signalisation cellulaire, en particulier lorsque les conditions métaboliques deviennent défavorables. Le coeur embryonnaire isolé représente donc un modèle expérimental utile pour mieux comprendre les mécanismes associés à une hypoxie in utero et pour améliorer les stratégies thérapeutiques en cardiologie et chirurgie foetales. ABSTRACT Physiopathology of the anoxic-reoxygenated embryonic heart: Protective role of NO and KATP channel Aim: In the adult heart, the electrical, mechanical, biochemical and structural disturbances induced by ischemia and reperfusion lead to reversible or irreversible damages depending on the severity and duration of ischemia. In spite of recent advances in fetal cardiology and surgery, little is known regarding the cellular mechanisms involved in hypoxia-induced dysfunction in the developing heart. The aim of this study was to precisely characterize the chrono-, dromo- and inotropic disturbances associated with anoxia-reoxygenation in an embryonic heart model. Furthermore, the roles that nitric oxide (NO), reactive oxygen species (ROS), mitochondrial KATP, (mito KATP) channel and MAP Kinases could play in the stressed developing heart have been investigated. Methods: Embryonic chick hearts (4-day-old) were isolated and submitted in vitro to 30 min anoxia followed by 60 min reoxygenation. Electrical (ECG) and contractile activities of atria, ventricle and conotruncus (photometric detection), ROS production (DCFH fluorescence) and ERK and JNK activity were determined in the ventricle throughout anoxia-reoxygenation. Hearts were treated with NO synthase inhibitor (L-NAME), NO donor (DETA-NONOate), mitoKATP channel opener (diazoxide) or blocket (5-HD), PKC inhibitor (chelerythrine) and ROS scavenger (MPG). Results: Anoxia and reoxygenation provoked arrhythxnias (mainly originating from atrial region), troubles of conduction (st, 2nd, and 3rd degree atrio-ventricular blocks) and disturbances of excitation-contraction (E-C) coupling. In addition to these types of arrhythmias, reoxygenation triggered Wenckebach phenomenon and rare ventricular escape beats. No fibrillations, no ventricular ectopic beats and no electromechanical dissociation were observed. Myocardial stunning was observed during the first 30 min of reoxygenation. All hearts fully recovered their electrical and mechanical functions after 30-40 min of reoxygenation. Exogenous NO improved while NOS inhibition delayed E-C coupling recovery. Mito KATP, channel opening increased reoxygenation-induced ROS production and improved E-C coupling and conduction (PR) recovery. MPG, chelerythrine or L-NAME reversed this effect. Reoxygenation increased ERK and JNK activities land 4-fold, respectively, while anoxia had no effect. MitoKATP channel opening abolished the reoxygenation-induced activation of JNK but had no effect on ERK activity. This inhibitory effect was partly reversed by mitoKATP channel blocker but not by MPG. Conclusion: In the developing heart, ventricular E-C coupling was found to be specially sensitive to hypoxia-reoxygenation and its postanoxic recovery was improved by mitoKATP channel activation via a ROS-, PKC- and NO-dependent pathway. JNK inhibition appears to be involved in this protection. Thus, mitochondria can play a pivotal role in the cellular signalling pathways, notably under critical metabolic conditions. The model of isolated embryonic heart appears to be useful to better understand the mechanisms underlying the myocardial dysfunction induced by an in utero hypoxia and to improve therapeutic strategies in fetal cardiology and surgery.

The biogeography of mitochondrial and nuclear discordance in animals.

Combining nuclear (nuDNA) and mitochondrial DNA (mtDNA) markers has improved the power of molecular data to test phylogenetic and phylogeographic hypotheses and has highlighted the limitations of studies using only mtDNA markers. In fact, in the past decade, many conflicting geographic patterns between mitochondrial and nuclear genetic markers have been identified (i.e. mito-nuclear discordance). Our goals in this synthesis are to: (i) review known cases of mito-nuclear discordance in animal systems, (ii) to summarize the biogeographic patterns in each instance and (iii) to identify common drivers of discordance in various groups. In total, we identified 126 cases in animal systems with strong evidence of discordance between the biogeographic patterns obtained from mitochondrial DNA and those observed in the nuclear genome. In most cases, these patterns are attributed to adaptive introgression of mtDNA, demographic disparities and sex-biased asymmetries, with some studies also implicating hybrid zone movement, human introductions and Wolbachia infection in insects. We also discuss situations where divergent mtDNA clades seem to have arisen in the absence of geographic isolation. For those cases where foreign mtDNA haplotypes are found deep within the range of a second taxon, data suggest that those mtDNA haplotypes are more likely to be at a high frequency and are commonly driven by sex-biased asymmetries and/or adaptive introgression. In addition, we discuss the problems with inferring the processes causing discordance from biogeographic patterns that are common in many studies. In many cases, authors presented more than one explanation for discordant patterns in a given system, which indicates that likely more data are required. Ideally, to resolve this issue, we see important future work shifting focus from documenting the prevalence of mito-nuclear discordance towards testing hypotheses regarding the drivers of discordance. Indeed, there is great potential for certain cases of mitochondrial introgression to become important natural systems within which to test the effect of different mitochondrial genotypes on whole-animal phenotypes.

Skeletal muscle mitochondrial and lipid droplet content assessed with standardized grid sizes for stereology.

Skeletal muscle mitochondrial (Mito) and lipid droplet (Lipid) content are often measured in human translational studies. Stereological point counting allows computing Mito and Lipid volume density (Vd) from micrographs taken with transmission electron microscopes. Former studies are not specific as to the size of individual squares that make up the grids, making reproducibility difficult, particularly when different magnifications are used. Our objective was to determine which size grid would be best at predicting fractional volume efficiently without sacrificing reliability and to test a novel method to reduce sampling bias. Methods: ten subjects underwent vastus lateralis biopsies. Samples were fixed, embedded, and cut longitudinally in ultrathin sections of 60 nm. Twenty micrographs from the intramyofibrillar region were taken per subject at Ã-33,000 magnification. Different grid sizes were superimposed on each micrograph: 1,000 Ã- 1,000 nm, 500 Ã- 500 nm, and 250 Ã- 250 nm. Results: mean Mito and Lipid Vd were not statistically different across grids. Variability was greater when going from 1,000 Ã- 1,000 to 500 Ã- 500 nm grid than from 500 Ã- 500 to 250 Ã- 250 nm grid. Discussion: this study is the first to attempt to standardize grid size while keeping with the conventional stereology principles. This is all in hopes of producing replicable assessments that can be obtained universally across different studies looking at human skeletal muscle mitochondrial and lipid droplet content.