Manifesto of artistic research: a defense against its advocates

Seit ihren Anfängen in den 1990er Jahren hat sich »künstlerische Forschung« als ein neues bildungs- und institutionenpolitisches wie auch ästhetisch-kunsttheoretisches Format etabliert. Inzwischen ist sie auf fast alle künstlerischen Felder diffundiert: von der Installationskunst über experimentelle Formate bis zur zeitgenössischen Musik, der Literatur oder Tanz- und Performancekunst. Doch steht sie seit ihrem Beginn – etikettiert unter Labels wie »Kunst und Wissenschaft« oder »Scienceart« und »Artscience«, die beide in einem Atemzug miteinander verbindet – im Wettstreit mit der akademischen Forschung, ohne dass ihr eigener Forschungsbegriff angemessen geklärt wäre. Das Manifest unternimmt den Versuch, Klärung zu schaffen und den Begriff, die Potenziale und Radikalität einer forschenden Kunst gegen diejenigen zu verteidigen, die allzu vorsichtig mit universitären Formaten liebäugeln und sie an wissenschaftliche Prinzipien anschließen wollen. Vielmehr geht es darum, die Eigenständigkeit und besondere Intellektualität ästhetischen Forschens herauszustreichen, ohne Legitimitätszwängen zu genügen und fremde Maßstäbe anzulegen

Pharmacokinetics and biodistribution of Erufosine in nude mice - implications for combination with radiotherapy

<p>Abstract</p> <p>Background</p> <p>Alkylphosphocholines represent promising antineoplastic drugs that induce cell death in tumor cells by primary interaction with the cell membrane. Recently we could show that a combination of radiotherapy with Erufosine, a paradigmatic intravenously applicable alkylphosphocholine, <it>in vitro </it>leads to a clear increase of irradiation-induced cell death. In view of a possible combination of Erufosine and radiotherapy <it>in vivo </it>we determined the pharmacokinetics and bioavailability as well as the tolerability of Erufosine in nude mice.</p> <p>Methods</p> <p>NMRI (nu/nu) nude mice were treated by intraperitoneal or subcutaneous injections of 5 to 40 mg/kg body weight Erufosine every 48 h for one to three weeks. Erufosine-concentrations were measured in brain, lungs, liver, small intestine, colon, spleen, kidney, stomach, adipoid tissue, and muscle by tandem-mass spectroscopy. Weight course, blood cell count and clinical chemistry were analyzed to evaluate general toxicity.</p> <p>Results</p> <p>Intraperitoneal injections were generally well tolerated in all dose groups but led to a transient loss of the bodyweight (<10%) in a dose dependent manner. Subcutaneous injections of high-dose Erufosine caused local reactions at the injection site. Therefore, this regimen at 40 mg/kg body weight Erufosine was stopped after 14 days. No gross changes were observed in organ weight, clinical chemistry and white blood cell count in treated compared to untreated controls except for a moderate increase in lactate dehydrogenase and aspartate-aminotransferase after intensive treatment. Repeated Erufosine injections resulted in drug-accumulation in different organs with maximum concentrations of about 1000 nmol/g in spleen, kidney and lungs.</p> <p>Conclusion</p> <p>Erufosine was well tolerated and organ-concentrations surpassed the cytotoxic drug concentrations <it>in vitro</it>. Our investigations establish the basis for a future efficacy testing of Erufosine in xenograft tumor models in nude mice alone and in combination with chemo- or radiotherapy.</p

Genomic analysis reveals key aspects of prokaryotic symbiosis in the phototrophic consortium "<em>Chlorochromatium aggregatum</em>"

BACKGROUND: ‘Chlorochromatium aggregatum’ is a phototrophic consortium, a symbiosis that may represent the highest degree of mutual interdependence between two unrelated bacteria not associated with a eukaryotic host. ‘Chlorochromatium aggregatum’ is a motile, barrel-shaped aggregate formed from a single cell of ‘Candidatus Symbiobacter mobilis”, a polarly flagellated, non-pigmented, heterotrophic bacterium, which is surrounded by approximately 15 epibiont cells of Chlorobium chlorochromatii, a non-motile photolithoautotrophic green sulfur bacterium. RESULTS: We analyzed the complete genome sequences of both organisms to understand the basis for this symbiosis. Chl. chlorochromatii has acquired relatively few symbiosis-specific genes; most acquired genes are predicted to modify the cell wall or function in cell-cell adhesion. In striking contrast, ‘Ca. S. mobilis’ appears to have undergone massive gene loss, is probably no longer capable of independent growth, and thus may only reproduce when consortia divide. A detailed model for the energetic and metabolic bases of the dependency of ‘Ca. S. mobilis’ on Chl. chlorochromatii is described. CONCLUSIONS: Genomic analyses suggest that three types of interactions lead to a highly sophisticated relationship between these two organisms. Firstly, extensive metabolic exchange, involving carbon, nitrogen, and sulfur sources as well as vitamins, occurs from the epibiont to the central bacterium. Secondly, ‘Ca. S. mobilis’ can sense and move towards light and sulfide, resources that only directly benefit the epibiont. Thirdly, electron cycling mechanisms, particularly those mediated by quinones and potentially involving shared protonmotive force, could provide an important basis for energy exchange in this and other symbiotic relationships

Impurity temperatures measured via line shape analysis in the island scrape-off-layer of Wendelstein 7-X

Impurity temperatures have been determined by a spectroscopic line shape analysis for several species in the divertor scrape-off-layer of the stellarator Wendelstein 7-X (W7-X). Examples include spectral lines from intrinsic elements (C II and C III, He I) as well as from seeded impurities (Ar II, N II) through the divertor gas inlet system. Both Doppler broadening and Zeeman splitting are found to contribute significantly to the impurity line shapes. Zeeman splitting arises due to the confining magnetic field in W7-X and complicates the line shape appearance. By attributing Doppler widths to each of the various Zeeman components, however, we demonstrate that reliable ion temperature values can be derived provided that the presence of the magnetic field is properly accounted for. The spectrally highly resolved lines are analyzed by means of a multi-parameter, least-squares fit routine, which accounts for Doppler broadening, Zeeman splitting, as well as the instrumental broadening of the spectrometer used to measure the spectral line shapes. By spectral fitting of the Zeeman features, it is also found that the line shape analysis can yield values for the local magnetic field, which can be used to localize the impurity radiation approximately provided that the line emission is dominant in a small area intersected by the lines of sight of the spectrometer

Deletion of the diabetes candidate gene Slc16a13 in mice attenuates diet-induced ectopic lipid accumulation and insulin resistance

Abstract Genome-wide association studies have identified SLC16A13 as a novel susceptibility gene for type 2 diabetes. The SLC16A13 gene encodes SLC16A13/MCT13, a member of the solute carrier 16 family of monocarboxylate transporters. Despite its potential importance to diabetes development, the physiological function of SLC16A13 is unknown. Here, we validate Slc16a13 as a lactate transporter expressed at the plasma membrane and report on the effect of Slc16a13 deletion in a mouse model. We show that loss of Slc16a13 increases mitochondrial respiration in the liver, leading to reduced hepatic lipid accumulation and increased hepatic insulin sensitivity in high-fat diet fed Slc16a13 knockout mice. We propose a mechanism for improved hepatic insulin sensitivity in the context of Slc16a13 deficiency in which reduced intrahepatocellular lactate availability drives increased AMPK activation and increased mitochondrial respiration, while reducing hepatic lipid content. Slc16a13 deficiency thereby attenuates hepatic diacylglycerol-PKCε mediated insulin resistance in obese mice. Together, these data suggest that SLC16A13 is a potential target for the treatment of type 2 diabetes and non-alcoholic fatty liver disease