‘Dark Tourism’ and the ‘Kitschification’ of 9/11

This paper aims to interrogate the framing of New York’s Ground Zero as a ‘dark tourist’ destination, with particular reference to the entanglement of notions of kitsch in academic discussions of the events of September 11th 2001. What makes Ground Zero contentious, even scandalous, for many scholars is the presence of a conspicuous commodity culture around the site in the form of tourist souvenirs, leading to accusations of kitschification of memory and the constitution of visitors as ‘tourists of history’. Drawing upon theoretical ideas of Jacques Ranciere, Bruno Latour and W. J. T. Mitchell around image politics, the alignment of kitsch with the figure of the tourist will be questioned, along with the conviction that the so-called ‘teddy-bearification’ of 9/11 threatens the formation of dangerous political subjectivities. In attempting to rid the debates of their default settings, and reliance on essentialist notions of kitsch, it is hoped that that the way will be cleared for the sociological, ethnographic and empirical work necessary to considering the cultural and political significance of the Ground Zero souvenir economy

Neue Möglichkeiten in der Therapie der hepatischen Enzephalopathie?

Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome associated with acute or chronic liver disease. It is generally considered a metabolic and potentially reversible syndrome. An important component of HE is increased neuro-inhibition caused by reduced hepatic metabolism of gut-derived nitrogenous substances and by activation of the postsynaptic GABAA-receptor complex in the central nervous system. Effective conventional therapy of HE includes prevention of precipitating factors, restriction of dietary protein an administration of lactulose (or lactitol) and possibly also of antibiotics. In addition, animal studies and uncontrolled clinical studies indicate that the benzodiazepine antagonist flumazenil effectively diminishes the increased neuroinhibition in certain patients with HE. However, these favourable flumazenil effects must be confirmed in larger randomized and placebo-controlled multicenter studies before flumazenil can be regarded as a useful new addition to current management of patients with acute or chronic hepatic encephalopathy

Effects of the benzodiazepine receptor antagonist flumazenil in hepatic encephalopathy in humans

If increased gamma-aminobutyric acid (GABA)-mediated neurotransmission contributes to the mediation of hepatic encephalopathy, it may be possible to induce ameliorations of the syndrome by pharmacologically antagonizing a component of the GABA/benzodiazepine receptor complex. To test this possibility we administered the benzodiazepine receptor antagonist flumazenil by intravenous injection to 14 patients with hepatic encephalopathy complicating cirrhosis. Flumazenil administration induced variable and transient, but distinct, improvements of the mental status in 71% of the patients. The degree of encephalopathy improved from stage IV to stage II in 4 patients and from stage IV to stage III in 2 patients. The mental status of all patients with less advanced encephalopathy (3 with stage III, 1 with stage II) also improved, but these responses were clinically less impressive. The arousal effect occurred within minutes after the injection and lasted for 1 to 2 h. Furthermore, it was associated with a significant increase of the mean electroencephalographic frequency from 4.2 to 5.2 cycle/s. Of the 8 patients who were ultimately discharged from the hospital, 7 had responded to flumazenil. No patient who died within 48 h of receiving flumazenil had shown any arousal effect. These findings strongly favor a prominent pathogenetic role of increased GABAergic tone in hepatic encephalopathy in humans and suggest that a positive response to flumazenil might be of prognostic value in predicting short-term survival in encephalopathic patients with liver disease

Effect of Flumazenil On Basal and Naloxone-Stimulated Acth and Cortisol Release in Humans

1. Endogenous benzodiazepine receptor ligands are thought to influence the human hypothalamic-pituitary-adrenal (HPA) axis and naloxone, a known stimulator of adrenocorticotropic hormone (ACTH) release, is thought to act via release of hypothalamic corticotropin-releasing hormone