TY - JOUR A1 - Kelly, U. A1 - Richter, S. A1 - Redenbach, C. A1 - Schladitz, K. A1 - Scheuerlein, C. A1 - Wolf, F. A1 - Ebermann, P. A1 - Lackner, F. A1 - Schoerling, D. A1 - Meinel, Dietmar T1 - Nb3Sn wire shape and cross sectional area inhomogeneity in Rutherford cables N2 - During Rutherford cable production the wires are plastically deformed and their initially round shape is distorted. Using X-ray absorption tomography we have determined the 3D shape of an unreacted Nb3Sn 11 T dipole Rutherford cable, and of a reacted and impregnated Nb3Sn cable double stack. State-of-theart image processing was applied to correct for tomographic artefacts caused by the large cable aspect ratio, for the segmentation of the individual wires and subelement bundles inside the wires, and for the calculation of the wire cross sectional area and shape variations. The 11 T dipole cable cross section oscillates by 2% with a frequency of 1.24 mm (1/80 of the transposition pitch length of the 40 wire cable). A comparatively stronger cross sectional area variation is observed in the individual wires at the thin edge of the keystoned cable where the wire aspect ratio is largest. KW - X-ray absorption tomography KW - Image processing KW - Accelerator magnet coils KW - Superconducting PY - 2018 DO - https://doi.org/10.1109/TASC.2018.2791637 SN - 1051-8223 SN - 1558-2515 VL - 28 IS - 4 SP - Article 4800705, 1 EP - 6 PB - IEEE Journals & Magazines AN - OPUS4-44556 LA - eng AD - Bundesanstalt fuer Materialforschung und -pruefung (BAM), Berlin, Germany ER - TY - JOUR A1 - Tjaden, B. A1 - Baum, K. A1 - Marquardt, V. A1 - Simon, M. A1 - Trajkovic-Arsic, M. A1 - Kouril, T. A1 - Siebers, B. A1 - Lisec, Jan A1 - Siveke, J. T. A1 - Schulte, J. H. A1 - Benary, U. A1 - Remke, M. A1 - Wolf, J. A1 - Schramm, A. T1 - MYCN-induced metabolic rewiring creates novel therapeutic vulnerabilities in neuroblastoma N2 - MYCN is a transcription factor that is aberrantly expressed in many tumor types and is often correlated with poor patient prognosis. Recently, several lines of evidence pointed to the fact that oncogenic activation of MYC family proteins is concomitant with reprogramming of tumor cells to cope with an enhanced need for metabolites during cell growth. These adaptions are driven by the ability of MYC proteins to act as transcriptional amplifiers in a tissue-of-origin specific manner. Here, we describe the effects of MYCN overexpression on metabolic reprogramming in neuroblastoma cells. Ectopic expression of MYCN induced a glycolytic switch that was concomitant with enhanced sensitivity towards 2-deoxyglucose, an inhibitor of glycolysis. Moreover, global metabolic profiling revealed extensive alterations in the cellular metabolome resulting from overexpression of MYCN. Limited supply with either of the two main carbon sources, glucose or glutamine, resulted in distinct shifts in steady-state metabolite levels and significant changes in glutathione metabolism. Interestingly, interference with glutamine-glutamate conversion preferentially blocked proliferation of MYCN overexpressing cells, when glutamine levels were reduced. Thus, our study uncovered MYCN induction and nutrient levels as important metabolic master switches in neuroblastoma cells and identified critical nodes that restrict tumor cell proliferation. KW - Mass-spectrometry KW - Tumor metabolism KW - MYCN PY - 2018 DO - https://doi.org/10.1101/423756 SP - 1 EP - 21 PB - Cold Spring Harbor Laboratory CY - Cold Spring Harbor, NY AN - OPUS4-46815 LA - eng AD - Bundesanstalt fuer Materialforschung und -pruefung (BAM), Berlin, Germany ER -