"...all diese fingierten, notierten, in meinem Kopf ungefähr wieder zusammengesetzten Ichs". Autobiographie und Autofiktion

Dass jede literarische Selbstdarstellung fiktionale Elemente beinhaltet, ist in der gegenwärtigen Autobiographie-Diskussion unbestritten. Mit dem von Serge Doubrovsky geprägten Terminus »Autofiktion« hat sich die Forschung verstärkt literarischen Texten zugewendet, die fiktionales und faktuales Erzählen der eigenen Biographie mehr oder minder offensichtlich vermischen und so die Problematik literarischer Selbstthematisierung reflektieren. Ausgehend von der theoretischen Diskussion um Autobiographie und Autofiktion werden Texte und Textentwürfe von Robert Walser, Annemarie Schwarzenbach, Paul Nizon, Friedrich Dürrenmatt und Urs Widmer mit ihren je eigenen und nicht selten eigenwilligen Konzepten des literarischen Umgangs mit der Biographie untersucht. Mit Beiträgen von Peter Gasser, Wolfram Groddeck, Lucas Marco Gisi, Heidy Margrit Müller, Ulrich Weber, Reto Sorg, Elio Pellin und Irmgard Wirtz.

Mutations in SDHD lead to autosomal recessive encephalomyopathy and isolated mitochondrial complex II deficiency

BACKGROUND Defects of the mitochondrial respiratory chain complex II (succinate dehydrogenase (SDH) complex) are extremely rare. Of the four nuclear encoded proteins composing complex II, only mutations in the 70 kDa flavoprotein (SDHA) and the recently identified complex II assembly factor (SDHAF1) have been found to be causative for mitochondrial respiratory chain diseases. Mutations in the other three subunits (SDHB, SDHC, SDHD) and the second assembly factor (SDHAF2) have so far only been associated with hereditary paragangliomas and phaeochromocytomas. Recessive germline mutations in SDHB have recently been associated with complex II deficiency and leukodystrophy in one patient. METHODS AND RESULTS We present the clinical and molecular investigations of the first patient with biochemical evidence of a severe isolated complex II deficiency due to compound heterozygous SDHD gene mutations. The patient presented with early progressive encephalomyopathy due to compound heterozygous p.E69 K and p.*164Lext*3 SDHD mutations. Native polyacrylamide gel electrophoresis and western blotting demonstrated an impaired complex II assembly. Complementation of a patient cell line additionally supported the pathogenicity of the novel identified mutations in SDHD. CONCLUSIONS This report describes the first case of isolated complex II deficiency due to recessive SDHD germline mutations. We therefore recommend screening for all SDH genes in isolated complex II deficiencies. It further emphasises the importance of appropriate genetic counselling to the family with regard to SDHD mutations and their role in tumorigenesis.

Percutaneous left-ventricular support with the Impella-2.5-assist device in acute cardiogenic shock: results of the Impella-EUROSHOCK-registry

BACKGROUND Acute cardiogenic shock after myocardial infarction is associated with high in-hospital mortality attributable to persisting low-cardiac output. The Impella-EUROSHOCK-registry evaluates the safety and efficacy of the Impella-2.5-percutaneous left-ventricular assist device in patients with cardiogenic shock after acute myocardial infarction. METHODS AND RESULTS This multicenter registry retrospectively included 120 patients (63.6±12.2 years; 81.7% male) with cardiogenic shock from acute myocardial infarction receiving temporary circulatory support with the Impella-2.5-percutaneous left-ventricular assist device. The primary end point evaluated mortality at 30 days. The secondary end point analyzed the change of plasma lactate after the institution of hemodynamic support, and the rate of early major adverse cardiac and cerebrovascular events as well as long-term survival. Thirty-day mortality was 64.2% in the study population. After Impella-2.5-percutaneous left-ventricular assist device implantation, lactate levels decreased from 5.8±5.0 mmol/L to 4.7±5.4 mmol/L (P=0.28) and 2.5±2.6 mmol/L (P=0.023) at 24 and 48 hours, respectively. Early major adverse cardiac and cerebrovascular events were reported in 18 (15%) patients. Major bleeding at the vascular access site, hemolysis, and pericardial tamponade occurred in 34 (28.6%), 9 (7.5%), and 2 (1.7%) patients, respectively. The parameters of age >65 and lactate level >3.8 mmol/L at admission were identified as predictors of 30-day mortality. After 317±526 days of follow-up, survival was 28.3%. CONCLUSIONS In patients with acute cardiogenic shock from acute myocardial infarction, Impella 2.5-treatment is feasible and results in a reduction of lactate levels, suggesting improved organ perfusion. However, 30-day mortality remains high in these patients. This likely reflects the last-resort character of Impella-2.5-application in selected patients with a poor hemodynamic profile and a greater imminent risk of death. Carefully conducted randomized controlled trials are necessary to evaluate the efficacy of Impella-2.5-support in this high-risk patient group.

Sex differences in the prevalence and clinical outcomes of subclinical peripheral artery disease in the Health, Aging, and Body Composition (Health ABC) study

The objective of the study was to determine if there are sex-based differences in the prevalence and clinical outcomes of subclinical peripheral artery disease (PAD). We evaluated the sex-specific associations of ankle-brachial index (ABI) with clinical cardiovascular disease outcomes in 2797 participants without prevalent clinical PAD and with a baseline ABI measurement in the Health, Aging, and Body Composition study. The mean age was 74 years, 40% were black, and 52% were women. Median follow-up was 9.37 years. Women had a similar prevalence of ABI < 0.9 (12% women versus 11% men; P = 0.44), but a higher prevalence of ABI 0.9-1.0 (15% versus 10%, respectively; P < 0.001). In a fully adjusted model, ABI < 0.9 was significantly associated with higher coronary heart disease (CHD) mortality, incident clinical PAD and incident myocardial infarction in both women and men. ABI < 0.9 was significantly associated with incident stroke only in women. ABI 0.9-1.0 was significantly associated with CHD death in both women (hazard ratio 4.84, 1.53-15.31) and men (3.49, 1.39-8.72). However, ABI 0.9-1.0 was significantly associated with incident clinical PAD (3.33, 1.44-7.70) and incident stroke (2.45, 1.38-4.35) only in women. Subclinical PAD was strongly associated with adverse CV events in both women and men, but women had a higher prevalence of subclinical PAD.

P2X7 receptors mediate resistance to toxin-induced cell lysis

In the majority of cells, the integrity of the plasmalemma is recurrently compromised by mechanical or chemical stress. Serum complement or bacterial pore-forming toxins can perforate the plasma membrane provoking uncontrolled Ca(2+) influx, loss of cytoplasmic constituents and cell lysis. Plasmalemmal blebbing has previously been shown to protect cells against bacterial pore-forming toxins. The activation of the P2X7 receptor (P2X7R), an ATP-gated trimeric membrane cation channel, triggers Ca(2+) influx and induces blebbing. We have investigated the role of the P2X7R as a regulator of plasmalemmal protection after toxin-induced membrane perforation caused by bacterial streptolysin O (SLO). Our results show that the expression and activation of the P2X7R furnishes cells with an increased chance of surviving attacks by SLO. This protective effect can be demonstrated not only in human embryonic kidney 293 (HEK) cells transfected with the P2X7R, but also in human mast cells (HMC-1), which express the receptor endogenously. In addition, this effect is abolished by treatment with blebbistatin or A-438079, a selective P2X7R antagonist. Thus blebbing, which is elicited by the ATP-mediated, paracrine activation of the P2X7R, is part of a cellular non-immune defense mechanism. It pre-empts plasmalemmal damage and promotes cellular survival. This mechanism is of considerable importance for cells of the immune system which carry the P2X7R and which are specifically exposed to toxin attacks.

Three decades of global methane sources and sinks

Methane is an important greenhouse gas, responsible for about 20 of the warming induced by long-lived greenhouse gases since pre-industrial times. By reacting with hydroxyl radicals, methane reduces the oxidizing capacity of the atmosphere and generates ozone in the troposphere. Although most sources and sinks of methane have been identified, their relative contributions to atmospheric methane levels are highly uncertain. As such, the factors responsible for the observed stabilization of atmospheric methane levels in the early 2000s, and the renewed rise after 2006, remain unclear. Here, we construct decadal budgets for methane sources and sinks between 1980 and 2010, using a combination of atmospheric measurements and results from chemical transport models, ecosystem models, climate chemistry models and inventories of anthropogenic emissions. The resultant budgets suggest that data-driven approaches and ecosystem models overestimate total natural emissions. We build three contrasting emission scenarios � which differ in fossil fuel and microbial emissions � to explain the decadal variability in atmospheric methane levels detected, here and in previous studies, since 1985. Although uncertainties in emission trends do not allow definitive conclusions to be drawn, we show that the observed stabilization of methane levels between 1999 and 2006 can potentially be explained by decreasing-to-stable fossil fuel emissions, combined with stable-to-increasing microbial emissions. We show that a rise in natural wetland emissions and fossil fuel emissions probably accounts for the renewed increase in global methane levels after 2006, although the relative contribution of these two sources remains uncertain.

Social milieus and worldviews in Mamluk adab-encyclopedias: The example of poverty and wealth

The economic and cultural rise of parts of the ʿāmma due to the particular economic and infrastructural conditions of the Mamluk era fostered the emergence of new intermediate levels of literature that were situated between the literature of the elite and that of the utterly ignorant and unlettered populace, between the Arabic koiné (al-ʿarabīya al-fuṣḥā) and the local dialects (ʿāmmīya-s), between written and oral composition, performance and transmission. The paper proposes to analyze the composition of three Mamluk adab-encyclopedias and their treatment of poverty and wealth in light of the social milieus of their authors and publics.

„Knallt‘s oder knallt‘s nicht?" - Dynamik der Gewalteskalation am Beispiel des Fussballstadions

Dynamik der Gewalteskalation bei kritischen Situationen am Beispiel des Fußballstadions Alain Brechbühl, Annemarie Schumacher-Dimech & Roland Seiler Institut für Sportwissenschaft, Universität Bern Schlüsselwörter: Zuschauergewalt, Wahrnehmung, Fußball, Massenveranstaltungen, Fan Einleitung Zuschauergewalt bei Fußballspielen ist in der Schweiz ein aktuelles Thema, wie etwa politische Debatten um Maßnahmen zur Prävention von Eskalationen zeigen. Während in anderen Ländern bereits verschiedene Studien durchgeführt wurden (bspw. Hylander & Granström, 2010), existiert in der Schweiz kaum Forschung zur Dynamik und den möglichen Faktoren, die den Unterschied zwischen einer Eskalation oder Nichteskalation ausmachen könnten. Insbesondere die Sicht beteiligter Personen ist dazu von entscheidender Bedeutung. Das vorliegende Projekt beschäftigt sich mit der subjektiv wahrgenommenen Gewaltsituation und deren zentralen Faktoren und Ursachen im Kontext des Fußballs. Methode Aufgrund der spärlichen Forschungslage in der Schweiz wurde eine explorative qualitative Studie mit involvierten und nichtinvolvierten Personen (Fußballfans, Sicherheitspersonal und die Polizei) durchgeführt, um Daten über kritische Situationen bei Spielen der Raiffeisen Super League zu erheben. Die ausgewählten Personen wurden einzeln mit narrativen Interviews zu der erlebten Situation befragt um genauere Erkenntnisse zur Situation zu erhalten. Zu vier Situationen wurden 34 Interviews durchgeführt (12 mit Polizeiangehörigen, 11 mit Fans, 9 mit Fanarbeitern und 2 mit Sicherheitsarbeitern). Die Auswertung erfolgte mit der interpretativen phänomenologischen Analyse. Ergebnisse Es zeigten sich individuelle und gruppenspezifische Wahrnehmungen in kritischen Situationen. Bei den befragten Personen herrschte häufig eine Tendenz zur (negativen) Stereotypisierung der gegenüberstehenden Gruppenmitglieder. Schnelle und klare Kommunikation, genügend Distanz zwischen den Gruppen und das Entfernen von gruppenspezifisch bedrohlichen Hinweisreizen (bspw. Polizei-Rüstungen) konnten als relevante Faktoren für gewaltfreie Lösungen festgestellt werden. Diskussion Die vorliegenden Ergebnisse sprechen für die Aufrechterhaltung einer differenzierten Betrachtungsweise und das Beiziehen von Vermittlungspersonen (von Fan- wie auch Polizeiseite) in kritischen Situationen, um Eskalationen vermeiden zu können. Es zeigen sich Ähnlichkeiten zu den Ergebnissen von Hylander & Granström (2010). Es werden noch weitere kritische Situationen analysiert, um konkrete Praxisempfehlungen zu formulieren. Literatur Hylander, I., & Granström, K. (2010). Organizing for a peaceful crowd: an example of a football match. Fo-rum Qualitative Social Research, 11 (2), Zugriff am 22.01.2014 unter http://www.qualitative-research.net/index.php/fqs/article/view/1462/2969.

Adolph Jellinek und die Kabbala : ein Literatur-Bericht

von I. M. Jost

Dealing with damage: Plasma membrane repair mechanisms.

Eukaryotic cells have developed repair mechanisms, which allow them to reseal their membrane in order to prevent the efflux of cytoplasmic constituents and the uncontrolled influx of calcium. After injury, the Ca(2+)-concentration gradient fulfils a dual function: it provides guidance cues for the repair machinery and directly activates the molecules, which have a repair function. Depending on the nature of injury, the morphology of the cell and the severity of injury, the membrane resealing can be effected by lysosomal exocytosis, microvesicle shedding or a combination of both. Likewise, exocytosis is often followed by the endocytic uptake of lesions. Additionally, since plasmalemmal resealing must be attempted, even after extensive injury in order to prevent cell lysis, the restoration of membrane integrity can be achieved by ceramide-driven invagination of the lipid bilayer, during which the cell is prepared for apoptotic disposal. Plasmalemmal injury can be contained by a surfeit of plasma membrane, which serves as a trap for toxic substances: either passively by an abundance of cellular protrusions, or actively by membrane blebbing.

Ca2+-dependent repair of pneumolysin pores: A new paradigm for host cellular defense against bacterial pore-forming toxins

Pneumolysin (PLY), a key virulence factor of Streptococcus pneumoniae, permeabilizes eukaryotic cells by forming large trans-membrane pores. PLY imposes a puzzling multitude of diverse, often mutually excluding actions on eukaryotic cells. Whereas cytotoxicity of PLY can be directly attributed to the pore-mediated effects, mechanisms that are responsible for the PLY-induced activation of host cells are poorly understood. We show that PLY pores can be repaired and thereby PLY-induced cell death can be prevented. Pore-induced Ca2+ entry from the extracellular milieu is of paramount importance for the initiation of plasmalemmal repair. Nevertheless, active Ca2+ sequestration that prevents excessive Ca2+ elevation during the execution phase of plasmalemmal repair is of no less importance. The efficacy of plasmalemmal repair does not only define the fate of targeted cells but also intensity, duration and repetitiveness of PLY-induced Ca2+ signals in cells that were able to survive after PLY attack. Intracellular Ca2+ dynamics evoked by the combined action of pore formation and their elimination mimic the pattern of receptor-mediated Ca2+ signaling, which is responsible for the activation of host immune responses. Therefore, we postulate that plasmalemmal repair of PLY pores might provoke cellular responses that are similar to those currently ascribed to the receptor-mediated PLY effects. Our data provide new insights into the understanding of the complexity of cellular non-immune defense responses to a major pneumococcal toxin that plays a critical role in the establishment and the progression of life-threatening diseases. Therapies boosting plasmalemmal repair of host cells and their metabolic fitness might prove beneficial for the treatment of pneumococcal infections.