TY  - JOUR
A1  - Abramowski, Attila
A1  - Aharonian, Felix A.
A1  - Benkhali, Faical  Ait
A1  - Akhperjanian, A. G.
A1  - Angüner, Ekrem Oǧuzhan
A1  - Backes, Michael
A1  - Balzer, Arnim
A1  - Becherini, Yvonne
A1  - Tjus, J. Becker
A1  - Berge, David
A1  - Bernhard, Sabrina
A1  - Bernlöhr, K.
A1  - Birsin, E.
A1  - Blackwell, R.
A1  - Boettcher, Markus
A1  - Boisson, Catherine
A1  - Bolmont, J.
A1  - Bordas, Pol
A1  - Bregeon, Johan
A1  - Brun, Francois
A1  - Brun, Pierre
A1  - Bryan, Mark
A1  - Bulik, Tomasz
A1  - Carr, John
A1  - Casanova, Sabrina
A1  - Chakraborty, N.
A1  - Chalme-Calvet, R.
A1  - Chaves, Ryan C. G.
A1  - Chen, Andrew
A1  - Chretien, M.
A1  - Colafrancesco, Sergio
A1  - Cologna, Gabriele
A1  - Conrad, Jan
A1  - Couturier, C.
A1  - Cui, Y.
A1  - Davids, I. D.
A1  - Degrange, B.
A1  - Deil, C.
A1  - deWilt, P.
A1  - Djannati-Ata, A.
A1  - Domainko, W.
A1  - Donath, A.
A1  - Dubus, G.
A1  - Dutson, K.
A1  - Dyks, J.
A1  - Dyrda, M.
A1  - Edwards, T.
A1  - Egberts, Kathrin
A1  - Eger, P.
A1  - Ernenwein, J-P.
A1  - Espigat, P.
A1  - Farnier, C.
A1  - Fegan, S.
A1  - Feinstein, F.
A1  - Fernandes, M. V.
A1  - Fernandez, D.
A1  - Fiasson, A.
A1  - Fontaine, G.
A1  - Foerster, A.
A1  - Fuessling, M.
A1  - Gabici, S.
A1  - Gajdus, M.
A1  - Gallant, Y. A.
A1  - Garrigoux, T.
A1  - Giavitto, G.
A1  - Giebels, B.
A1  - Glicenstein, J. F.
A1  - Gottschall, D.
A1  - Goyal, A.
A1  - Grondin, M-H.
A1  - Grudzinska, M.
A1  - Hadasch, D.
A1  - Haeffner, S.
A1  - Hahn, J.
A1  - Hawkes, J.
A1  - Heinzelmann, G.
A1  - Henri, G.
A1  - Hermann, G.
A1  - Hervet, O.
A1  - Hillert, A.
A1  - Hinton, James Anthony
A1  - Hofmann, W.
A1  - Hofverberg, P.
A1  - Hoischen, Clemens
A1  - Holler, M.
A1  - Horns, D.
A1  - Ivascenko, A.
A1  - Jacholkowska, A.
A1  - Jamrozy, M.
A1  - Janiak, M.
A1  - Jankowsky, F.
A1  - Jung-Richardt, I.
A1  - Kastendieck, M. A.
A1  - Katarzynski, K.
A1  - Katz, U.
A1  - Kerszberg, D.
A1  - Khelifi, B.
A1  - Kieffer, M.
A1  - Klepser, S.
A1  - Klochkov, D.
A1  - Kluzniak, W.
A1  - Kolitzus, D.
A1  - Komin, Nu.
A1  - Kosack, K.
A1  - Krakau, S.
A1  - Krayzel, F.
A1  - Krueger, P. P.
A1  - Laffon, H.
A1  - Lamanna, G.
A1  - Lau, J.
A1  - Lefaucheur, J.
A1  - Lefranc, V.
A1  - Lemiere, A.
A1  - Lemoine-Goumard, M.
A1  - Lenain, J-P.
A1  - Lohse, T.
A1  - Lopatin, A.
A1  - Lu, C-C.
A1  - Lui, R.
A1  - Marandon, V.
A1  - Marcowith, A.
A1  - Mariaud, C.
A1  - Marx, R.
A1  - Maurin, G.
A1  - Maxted, N.
A1  - Mayer, M.
A1  - Meintjes, P. J.
A1  - Menzler, U.
A1  - Meyer, M.
A1  - Mitchell, A. M. W.
A1  - Moderski, R.
A1  - Mohamed, M.
A1  - Mora, K.
A1  - Moulin, E.
A1  - Murach, T.
A1  - de Naurois, M.
A1  - Niemiec, J.
A1  - Oakes, L.
A1  - Odaka, H.
A1  - Oettl, S.
A1  - Ohm, S.
A1  - Opitz, B.
A1  - Ostrowski, M.
A1  - Oya, I.
A1  - Panter, M.
A1  - Parsons, R. D.
A1  - Arribas, M. Paz
A1  - Pekeur, N. W.
A1  - Pelletier, G.
A1  - Petrucci, P-O.
A1  - Peyaud, B.
A1  - Pita, S.
A1  - Poon, H.
A1  - Prokoph, H.
A1  - Puehlhofer, G.
A1  - Punch, M.
A1  - Quirrenbach, A.
A1  - Raab, S.
A1  - Reichardt, I.
A1  - Reimer, A.
A1  - Reimer, O.
A1  - Renaud, M.
A1  - de los Reyes, R.
A1  - Rieger, F.
A1  - Romoli, C.
A1  - Rosier-Lees, S.
A1  - Rowell, G.
A1  - Rudak, B.
A1  - Rulten, C. B.
A1  - Sahakian, V.
A1  - Salek, D.
A1  - Sanchez, David M.
A1  - Santangelo, A.
A1  - Sasaki, M.
A1  - Schlickeiser, R.
A1  - Schuessler, F.
A1  - Schulz, A.
A1  - Schwanke, U.
A1  - Schwemmer, S.
A1  - Seyffert, A. S.
A1  - Simoni, R.
A1  - Sol, H.
A1  - Spanier, F.
A1  - Spengler, G.
A1  - Spies, F.
A1  - Stawarz, L.
A1  - Steenkamp, R.
A1  - Stegmann, Christian
A1  - Stinzing, F.
A1  - Stycz, K.
A1  - Sushch, Iurii
A1  - Tavernet, J-P.
A1  - Tavernier, T.
A1  - Taylor, A. M.
A1  - Terrier, R.
A1  - Tluczykont, M.
A1  - Trichard, C.
A1  - Tuffs, R.
A1  - Valerius, K.
A1  - van der Walt, J.
A1  - van Eldik, C.
A1  - van Soelen, B.
A1  - Vasileiadis, G.
A1  - Veh, J.
A1  - Venter, C.
A1  - Viana, A.
A1  - Vincent, P.
A1  - Vink, J.
A1  - Voisin, F.
A1  - Voelk, H. J.
A1  - Vuillaume, T.
A1  - Wagner, S. J.
A1  - Wagner, P.
A1  - Wagner, R. M.
A1  - Weidinger, M.
A1  - Weitzel, Q.
A1  - White, R.
A1  - Wierzcholska, A.
A1  - Willmann, P.
A1  - Woernlein, A.
A1  - Wouters, D.
A1  - Yang, R.
A1  - Zabalza, V.
A1  - Zaborov, D.
A1  - Zacharias, M.
A1  - Zdziarski, A. A.
A1  - Zech, Alraune
A1  - Zefi, F.
A1  - Zywucka, N.
T1  - Acceleration of petaelectronvolt protons in the Galactic Centre
JF  - Nature : the international weekly journal of science
N2  - Galactic cosmic rays reach energies of at least a few petaelectronvolts (of the order of 1015 electronvolts). This implies that our Galaxy contains petaelectronvolt accelerators (‘PeVatrons’), but all proposed models of Galactic cosmic-ray accelerators encounter difficulties at exactly these energies. Dozens of Galactic accelerators capable of accelerating particles to energies of tens of teraelectronvolts (of the order of 1013 electronvolts) were inferred from recent γ-ray observations3. However, none of the currently known accelerators—not even the handful of shell-type supernova remnants commonly believed to supply most Galactic cosmic rays—has shown the characteristic tracers of petaelectronvolt particles, namely, power-law spectra of γ-rays extending without a cut-off or a spectral break to tens of teraelectronvolts4. Here we report deep γ-ray observations with arcminute angular resolution of the region surrounding the Galactic Centre, which show the expected tracer of the presence of petaelectronvolt protons within the central 10 parsecs of the Galaxy. We propose that the supermassive black hole Sagittarius A* is linked to this PeVatron. Sagittarius A* went through active phases in the past, as demonstrated by X-ray outbursts5and an outflow from the Galactic Centre6. Although its current rate of particle acceleration is not sufficient to provide a substantial contribution to Galactic cosmic rays, Sagittarius A* could have plausibly been more active over the last 106–107 years, and therefore should be considered as a viable alternative to supernova remnants as a source of petaelectronvolt Galactic cosmic rays.
Y1  - 2016
U6  - https://doi.org/10.1038/nature17147
SN  - 0028-0836
SN  - 1476-4687
VL  - 531
SP  - 476
EP  - +
PB  - Nature Publ. Group
CY  - London
ER  - 
TY  - JOUR
A1  - Beckmann, Nadine
A1  - Becker, Katrin Anne
A1  - Kadow, Stephanie
A1  - Schumacher, Fabian
A1  - Kramer, Melanie
A1  - Kuehn, Claudine
A1  - Schulz-Schaeffer, Walter J.
A1  - Edwards, Michael J.
A1  - Kleuser, Burkhard
A1  - Gulbins, Erich
A1  - Carpinteiro, Alexander
T1  - Acid Sphingomyelinase Deficiency Ameliorates Farber Disease
JF  - International journal of molecular sciences
N2  - Farber disease is a rare lysosomal storage disorder resulting from acid ceramidase deficiency and subsequent ceramide accumulation. No treatments for Farber disease are clinically available, and affected patients have a severely shortened lifespan. We have recently reported a novel acid ceramidase deficiency model that mirrors the human disease closely. Acid sphingomyelinase is the enzyme that generates ceramide upstream of acid ceramidase in the lysosomes. Using our acid ceramidase deficiency model, we tested if acid sphingomyelinase could be a potential novel therapeutic target for the treatment of Farber disease. A number of functional acid sphingomyelinase inhibitors are clinically available and have been used for decades to treat major depression. Using these as a therapeutic for Farber disease, thus, has the potential to improve central nervous symptoms of the disease as well, something all other treatment options for Farber disease can’t achieve so far. As a proof-of-concept study, we first cross-bred acid ceramidase deficient mice with acid sphingomyelinase deficient mice in order to prevent ceramide accumulation. Double-deficient mice had reduced ceramide accumulation, fewer disease manifestations, and prolonged survival. We next targeted acid sphingomyelinase pharmacologically, to test if these findings would translate to a setting with clinical applicability. Surprisingly, the treatment of acid ceramidase deficient mice with the acid sphingomyelinase inhibitor amitriptyline was toxic to acid ceramidase deficient mice and killed them within a few days of treatment. In conclusion, our study provides the first proof-of-concept that acid sphingomyelinase could be a potential new therapeutic target for Farber disease to reduce disease manifestations and prolong survival. However, we also identified previously unknown toxicity of the functional acid sphingomyelinase inhibitor amitriptyline in the context of Farber disease, strongly cautioning against the use of this substance class for Farber disease patients.
KW  - Farber disease
KW  - lysosomal storage disorders
KW  - acid ceramidase
KW  - acid sphingomyelinase
KW  - amitriptyline
Y1  - 2019
U6  - https://doi.org/10.3390/ijms20246253
SN  - 1422-0067
VL  - 20
IS  - 24
PB  - MDPI
CY  - Basel
ER  - 
TY  - GEN
A1  - Beckmann, Nadine
A1  - Becker, Katrin Anne
A1  - Kadow, Stephanie
A1  - Schumacher, Fabian
A1  - Kramer, Melanie
A1  - Kühn, Claudine
A1  - Schulz-Schaeffer, Walter J.
A1  - Edwards, Michael J.
A1  - Kleuser, Burkhard
A1  - Gulbins, Erich
A1  - Carpinteiro, Alexander
T1  - Acid sphingomyelinase deficiency ameliorates Farber disease
T2  - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe
N2  - Farber disease is a rare lysosomal storage disorder resulting from acid ceramidase deficiency and subsequent ceramide accumulation. No treatments for Farber disease are clinically available, and affected patients have a severely shortened lifespan. We have recently reported a novel acid ceramidase deficiency model that mirrors the human disease closely. Acid sphingomyelinase is the enzyme that generates ceramide upstream of acid ceramidase in the lysosomes. Using our acid ceramidase deficiency model, we tested if acid sphingomyelinase could be a potential novel therapeutic target for the treatment of Farber disease. A number of functional acid sphingomyelinase inhibitors are clinically available and have been used for decades to treat major depression. Using these as a therapeutic for Farber disease, thus, has the potential to improve central nervous symptoms of the disease as well, something all other treatment options for Farber disease can’t achieve so far. As a proof-of-concept study, we first cross-bred acid ceramidase deficient mice with acid sphingomyelinase deficient mice in order to prevent ceramide accumulation. Double-deficient mice had reduced ceramide accumulation, fewer disease manifestations, and prolonged survival. We next targeted acid sphingomyelinase pharmacologically, to test if these findings would translate to a setting with clinical applicability. Surprisingly, the treatment of acid ceramidase deficient mice with the acid sphingomyelinase inhibitor amitriptyline was toxic to acid ceramidase deficient mice and killed them within a few days of treatment. In conclusion, our study provides the first proof-of-concept that acid sphingomyelinase could be a potential new therapeutic target for Farber disease to reduce disease manifestations and prolong survival. However, we also identified previously unknown toxicity of the functional acid sphingomyelinase inhibitor amitriptyline in the context of Farber disease, strongly cautioning against the use of this substance class for Farber disease patients
T3  - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 1087 
KW  - Farber disease
KW  - lysosomal storage disorders
KW  - acid ceramidase
KW  - acid sphingomyelinase
KW  - amitriptyline
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-441282
SN  - 1866-8372
IS  - 1087
ER  - 
TY  - JOUR
A1  - Gulbins, Erich
A1  - Palmada, Monica
A1  - Reichel, Martin
A1  - Lueth, Anja
A1  - Boehmer, Christoph
A1  - Amato, Davide
A1  - Mueller, Christian P.
A1  - Tischbirek, Carsten H.
A1  - Groemer, Teja W.
A1  - Tabatabai, Ghazaleh
A1  - Becker, Katrin Anne
A1  - Tripal, Philipp
A1  - Staedtler, Sven
A1  - Ackermann, Teresa F.
A1  - van Brederode, Johannes
A1  - Alzheimer, Christian
A1  - Weller, Michael
A1  - Lang, Undine E.
A1  - Kleuser, Burkhard
A1  - Grassme, Heike
A1  - Kornhuber, Johannes
T1  - Acid sphingomyelinase-ceramide system mediates effects of antidepressant drugs
JF  - Nature medicine
N2  - Major depression is a highly prevalent severe mood disorder that is treated with antidepressants. The molecular targets of antidepressants require definition. We investigated the role of the acid sphingomyelinase (Asm)-ceramide system as a target for antidepressants. Therapeutic concentrations of the antidepressants amitriptyline and fluoxetine reduced Asm activity and ceramide concentrations in the hippocampus, increased neuronal proliferation, maturation and survival and improved behavior in mouse models of stress-induced depression. Genetic Asm deficiency abrogated these effects. Mice overexpressing Asm, heterozygous for acid ceramidase, treated with blockers of ceramide metabolism or directly injected with C16 ceramide in the hippocampus had higher ceramide concentrations and lower rates of neuronal proliferation, maturation and survival compared with controls and showed depression-like behavior even in the absence of stress. The decrease of ceramide abundance achieved by antidepressant-mediated inhibition of Asm normalized these effects. Lowering ceramide abundance may thus be a central goal for the future development of antidepressants.
Y1  - 2013
U6  - https://doi.org/10.1038/nm.3214
SN  - 1078-8956
VL  - 19
IS  - 7
SP  - 934
EP  - +
PB  - Nature Publ. Group
CY  - New York
ER  - 
TY  - JOUR
A1  - Gulbins, Anne
A1  - Schumacher, Fabian
A1  - Becker, Katrin Anne
A1  - Wilker, Barbara
A1  - Soddemann, Matthias
A1  - Boldrin, Francesco
A1  - Müller, Christian P.
A1  - Edwards, Michael J.
A1  - Goodman, Michael
A1  - Caldwell, Charles C.
A1  - Kleuser, Burkhard
A1  - Kornhuber, Johannes
A1  - Szabo, Ildiko
A1  - Gulbins, Erich
T1  - Antidepressants act by inducing autophagy controlled by sphingomyelin-ceramide
JF  - Molecular psychiatry
N2  - Major depressive disorder (MDD) is a common and severe disease characterized by mood changes, somatic alterations, and often suicide. MDD is treated with antidepressants, but the molecular mechanism of their action is unknown. We found that widely used antidepressants such as amitriptyline and fluoxetine induce autophagy in hippocampal neurons via the slow accumulation of sphingomyelin in lysosomes and Golgi membranes and of ceramide in the endoplasmic reticulum (ER). ER ceramide stimulates phosphatase 2A and thereby the autophagy proteins Ulk, Beclin, Vps34/Phosphatidylinositol 3-kinase, p62, and Lc3B. Although treatment with amitriptyline or fluoxetine requires at least 12 days to achieve sphingomyelin accumulation and the subsequent biochemical and cellular changes, direct inhibition of sphingomyelin synthases with tricyclodecan-9-yl-xanthogenate (D609) results in rapid (within 3 days) accumulation of ceramide in the ER, activation of autophagy, and reversal of biochemical and behavioral signs of stress-induced MDD. Inhibition of Beclin blocks the antidepressive effects of amitriptyline and D609 and induces cellular and behavioral changes typical of MDD. These findings identify sphingolipid-controlled autophagy as an important target for antidepressive treatment methods and provide a rationale for the development of novel antidepressants that act within a few days.
Y1  - 2018
U6  - https://doi.org/10.1038/s41380-018-0090-9
SN  - 1359-4184
SN  - 1476-5578
VL  - 23
IS  - 12
SP  - 2324
EP  - 2346
PB  - Nature Publ. Group
CY  - London
ER  - 
TY  - JOUR
A1  - Abdalla, H.
A1  - Abramowski, A.
A1  - Aharonian, Felix A.
A1  - Benkhali, F. Ait
A1  - Akhperjanian, A. G.
A1  - Andersson, T.
A1  - Anguener, E. O.
A1  - Arrieta, M.
A1  - Aubert, P.
A1  - Backes, M.
A1  - Balzer, A.
A1  - Barnard, M.
A1  - Becherini, Y.
A1  - Tjus, J. Becker
A1  - Berge, D.
A1  - Bernhard, S.
A1  - Bernlorhr, K.
A1  - Blackwell, R.
A1  - Bottcher, M.
A1  - Boisson, C.
A1  - Bolmont, J.
A1  - Bordas, Pol
A1  - Bregeon, J.
A1  - Brun, F.
A1  - Brun, P.
A1  - Bryan, M.
A1  - Bulik, T.
A1  - Capasso, M.
A1  - Carr, J.
A1  - Casanova, Sabrina
A1  - Cerruti, M.
A1  - Chakraborty, N.
A1  - Chalme-Calvet, R.
A1  - Chaves, R. C. G.
A1  - Chen, A.
A1  - Chevalier, J.
A1  - Chretien, M.
A1  - Colafrancesco, S.
A1  - Cologna, G.
A1  - Condon, B.
A1  - Conrad, J.
A1  - Cui, Y.
A1  - Davids, I. D.
A1  - Decock, J.
A1  - Degrange, B.
A1  - Deil, C.
A1  - Devin, J.
A1  - deWilt, P.
A1  - Dirson, L.
A1  - Djannati-Atai, A.
A1  - Domainko, W.
A1  - Donath, A.
A1  - Dubus, G.
A1  - Dutson, K.
A1  - Dyks, J.
A1  - Edwards, T.
A1  - Egberts, Kathrin
A1  - Eger, P.
A1  - Ernenwein, J. -P.
A1  - Eschbach, S.
A1  - Farnier, C.
A1  - Fegan, S.
A1  - Fernandes, M. V.
A1  - Fiasson, A.
A1  - Fontaine, G.
A1  - Foerster, A.
A1  - Funk, S.
A1  - Fuessling, M.
A1  - Gabici, S.
A1  - Gajdus, M.
A1  - Gallant, Y. A.
A1  - Garrigoux, T.
A1  - Giavitto, G.
A1  - Giebels, B.
A1  - Glicenstein, J. F.
A1  - Gottschall, D.
A1  - Goyal, A.
A1  - Grondin, M. -H.
A1  - Hadasch, D.
A1  - Hahn, J.
A1  - Haupt, M.
A1  - Hawkes, J.
A1  - Heinzelmann, G.
A1  - Henri, G.
A1  - Hermann, G.
A1  - Hervet, O.
A1  - Hinton, J. A.
A1  - Hofmann, W.
A1  - Hoischen, Clemens
A1  - Holler, M.
A1  - Horns, D.
A1  - Ivascenko, A.
A1  - Jacholkowska, A.
A1  - Jamrozy, M.
A1  - Janiak, M.
A1  - Jankowsky, D.
A1  - Jankowsky, F.
A1  - Jingo, M.
A1  - Jogler, T.
A1  - Jouvin, L.
A1  - Jung-Richardt, I.
A1  - Kastendieck, M. A.
A1  - Katarzynski, K.
A1  - Katz, U.
A1  - Kerszberg, D.
A1  - Khelifi, B.
A1  - Er, M. Kie Ff
A1  - King, J.
A1  - Klepser, S.
A1  - Klochkov, D.
A1  - Kluzniak, W.
A1  - Kolitzus, D.
A1  - Komin, Nu.
A1  - Kosack, K.
A1  - Krakau, S.
A1  - Kraus, M.
A1  - Krayzel, F.
A1  - Kruger, P. P.
A1  - Laffon, H.
A1  - Lamanna, G.
A1  - Lau, J.
A1  - Lees, J. -P.
A1  - Lefaucheur, J.
A1  - Lefranc, V.
A1  - Lemiere, A.
A1  - Lemoine-Goumard, M.
A1  - Lenain, J. -P.
A1  - Leser, E.
A1  - Lohse, T.
A1  - Lorentz, M.
A1  - Liu, R.
A1  - Lopez-Coto, R.
A1  - Lypova, I.
A1  - Marandon, V.
A1  - Marcowith, A.
A1  - Mariaud, C.
A1  - Marx, R.
A1  - Maurin, G.
A1  - Maxted, N.
A1  - Mayer, M.
A1  - Meintjes, P. J.
A1  - Meyer, M.
A1  - Mitchell, A. M. W.
A1  - Moderski, R.
A1  - Mohamed, M.
A1  - Mohrmann, L.
A1  - Mora, K.
A1  - Moulin, E.
A1  - Murach, T.
A1  - de Naurois, M.
A1  - Niederwanger, F.
A1  - Niemiec, J.
A1  - Oakes, L.
A1  - Odaka, H.
A1  - Oettl, S.
A1  - Ohm, S.
A1  - Ostrowski, M.
A1  - Oya, I.
A1  - Padovani, M.
A1  - Panter, M.
A1  - Parsons, R. D.
A1  - Pekeur, N. W.
A1  - Pelletier, G.
A1  - Perennes, C.
A1  - Petrucci, P. -O.
A1  - Peyaud, B.
A1  - Piel, Q.
A1  - Pita, S.
A1  - Poon, H.
A1  - Prokhorov, D.
A1  - Prokoph, H.
A1  - Puehlhofer, G.
A1  - Punch, M.
A1  - Quirrenbach, A.
A1  - Raab, S.
A1  - Reimer, A.
A1  - Reimer, O.
A1  - Renaud, M.
A1  - de los Reyes, R.
A1  - Rieger, F.
A1  - Romoli, C.
A1  - Rosier-Lees, S.
A1  - Rowell, G.
A1  - Rudak, B.
A1  - Rulten, C. B.
A1  - Sahakian, V.
A1  - Salek, D.
A1  - Sanchez, D. A.
A1  - Santangelo, A.
A1  - Sasaki, M.
A1  - Schlickeiser, R.
A1  - Schussler, F.
A1  - Schulz, A.
A1  - Schwanke, U.
A1  - Schwemmer, S.
A1  - Settimo, M.
A1  - Seyffert, A. S.
A1  - Shafi, N.
A1  - Shilon, I.
A1  - Simoni, R.
A1  - Sol, H.
A1  - Spanier, F.
A1  - Spengler, G.
A1  - Spies, F.
A1  - Ert, Ff
A1  - Stawarz, L.
A1  - Steenkamp, R.
A1  - Stegmann, Christian Michael
A1  - Stinzing, F.
A1  - Stycz, K.
A1  - Sushch, I.
A1  - Tavernet, J. -P.
A1  - Tavernier, T.
A1  - Taylor, A. M.
A1  - Terrier, R.
A1  - Tibaldo, L.
A1  - Tiziani, D.
A1  - Tluczykont, M.
A1  - Trichard, C.
A1  - Tuffs, R.
A1  - Uchiyama, Y.
A1  - van der Walt, D. J.
A1  - van Eldik, C.
A1  - van Rensburg, C.
A1  - van Soelen, B.
A1  - Vasileiadis, G.
A1  - Veh, J.
A1  - Venter, C.
A1  - Viana, A.
A1  - Vincent, P.
A1  - Vink, J.
A1  - Voisin, F.
A1  - Voelk, H. J.
A1  - Vuillaume, T.
A1  - Wadiasingh, Z.
A1  - Wagner, S. J.
A1  - Wagner, P.
A1  - Wagner, R. M.
A1  - White, R.
A1  - Wierzcholska, A.
A1  - Willmann, P.
A1  - Woernlein, A.
A1  - Wouters, D.
A1  - Yang, R.
A1  - Zabalza, V.
A1  - Zaborov, D.
A1  - Zacharias, M.
A1  - Zdziarski, A. A.
A1  - Zech, Alraune
A1  - Zefi, F.
A1  - Ziegler, A.
A1  - Zywucka, N.
T1  - Characterizing the gamma-ray long-term variability of PKS2155 304 with HESS and Fermi-LAT
JF  - Astronomy and astrophysics : an international weekly journal
N2  - Studying the temporal variability of BL Lac objects at the highest energies provides unique insights into the extreme physical processes occurring in relativistic jets and in the vicinity of super-massive black holes. To this end, the long-term variability of the BL Lac object PKS 2155 304 is analyzed in the high (HE, 100MeV < E < 300 GeV) and very high energy (VHE, E > 200 GeV) gamma-ray domain. Over the course of similar to 9 yr of H. E. S. S. observations the VHE light curve in the quiescent state is consistent with a log-normal behavior. The VHE variability in this state is well described by flicker noise (power-spectral-density index beta(VHE) = 1 .10(+ 0 : 10) (0 : 13)) on timescales larger than one day. An analysis of similar to 5.5 yr of HE Fermi-LAT data gives consistent results (beta(HE) = 1 : 20(+ 0 : 21) (0 : 23), on timescales larger than 10 days) compatible with the VHE findings. The HE and VHE power spectral densities show a scale invariance across the probed time ranges. A direct linear correlation between the VHE and HE fluxes could neither be excluded nor firmly established. These long-term-variability properties are discussed and compared to the red noise behavior (beta similar to 2) seen on shorter timescales during VHE-flaring states. The difference in power spectral noise behavior at VHE energies during quiescent and flaring states provides evidence that these states are influenced by different physical processes, while the compatibility of the HE and VHE long-term results is suggestive of a common physical link as it might be introduced by an underlying jet-disk connection.
KW  - galaxies: active
KW  - BL Lacertae objects: individual: PKS 2155-304
KW  - gamma rays: galaxies
KW  - galaxies: jets
KW  - galaxies: nuclei
KW  - radiation mechanisms: non-thermal
Y1  - 2017
U6  - https://doi.org/10.1051/0004-6361/201629419
SN  - 1432-0746
SN  - 0004-6361
VL  - 598
PB  - EDP Sciences
CY  - Les Ulis
ER  - 
TY  - JOUR
A1  - Dumont, Hanna
A1  - Neumann, Marko
A1  - Nagy, Gabriel
A1  - Becker, Michael
A1  - Rose, Norman
A1  - Trautwein, Ulrich
T1  - Class composition Effects in non-academic lower secondary school tracks in the state of Baden-Württemberg
JF  - Psychologie in Erziehung und Unterricht : Zeitschrift für Forschung und Praxis
N2  - The study investigates the effects of classroom composition (average ability, achievement, and socio-economic background, proportion of immigrant students) on the development in mathematics achievement, and reading literacy from grade 5 to 6. The study draws on a sample of N=1892 students in vocational track schools (Hauptschule) and intermediate track schools (Realschule) in Baden-Wuerttemberg, Germany. After controlling for school type, and between-school differences in student intake characteristics, none of the compositional characteristics showed a statistically significant effect on achievement development. School track was associated with the development of reading literacy even after controlling for individual differences; however, this relationship lost its statistical significance after the composition of the student body was additionally taken into account.
KW  - Academic achievement
KW  - tracking
KW  - reading comprehension
KW  - mathematics
KW  - composition effects
Y1  - 2013
U6  - https://doi.org/10.2378/peu2013.art16d
SN  - 0342-183X
VL  - 60
IS  - 3
SP  - 198
EP  - 213
PB  - Reinhardt
CY  - München
ER  - 
TY  - JOUR
A1  - Abramowski, Attila
A1  - Aharonian, Felix A.
A1  - Benkhali, Faical  Ait
A1  - Akhperjanian, A. G.
A1  - Angüner, Ekrem Oǧuzhan
A1  - Backes, Michael
A1  - Balenderan, Shangkari
A1  - Balzer, Arnim
A1  - Barnacka, Anna
A1  - Becherini, Yvonne
A1  - Tjus, J. Becker
A1  - Berge, David
A1  - Bernhard, Sabrina
A1  - Bernlöhr, K.
A1  - Birsin, E.
A1  - Biteau, Jonathan
A1  - Boettcher, Markus
A1  - Boisson, Catherine
A1  - Bolmont, J.
A1  - Bordas, Pol
A1  - Bregeon, Johan
A1  - Brun, Francois
A1  - Brun, Pierre
A1  - Bryan, Mark
A1  - Bulik, Tomasz
A1  - Carrigan, Svenja
A1  - Casanova, Sabrina
A1  - Chadwick, Paula M.
A1  - Chakraborty, N.
A1  - Chalme-Calvet, R.
A1  - Chaves, Ryan C. G.
A1  - Chretien, M.
A1  - Colafrancesco, Sergio
A1  - Cologna, Gabriele
A1  - Conrad, Jan
A1  - Couturier, C.
A1  - Cui, Y.
A1  - Davids, I. D.
A1  - Degrange, B.
A1  - Deil, C.
A1  - deWilt, P.
A1  - Djannati-Ataï, A.
A1  - Domainko, W.
A1  - Donath, A.
A1  - Dubus, G.
A1  - Dutson, K.
A1  - Dyks, J.
A1  - Dyrda, M.
A1  - Edwards, T.
A1  - Egberts, Kathrin
A1  - Eger, P.
A1  - Espigat, P.
A1  - Farnier, C.
A1  - Fegan, S.
A1  - Feinstein, F.
A1  - Fernandes, M. V.
A1  - Fernandez, D.
A1  - Fiasson, A.
A1  - Fontaine, G.
A1  - Foerster, A.
A1  - Fuessling, M.
A1  - Gabici, S.
A1  - Gajdus, M.
A1  - Gallant, Y. A.
A1  - Garrigoux, T.
A1  - Giavitto, G.
A1  - Giebels, B.
A1  - Glicenstein, J. F.
A1  - Gottschall, D.
A1  - Grondin, M. -H.
A1  - Grudzinska, M.
A1  - Hadasch, D.
A1  - Haeffner, S.
A1  - Hahn, J.
A1  - Harris, J.
A1  - Heinzelmann, G.
A1  - Henri, G.
A1  - Hermann, G.
A1  - Hervet, O.
A1  - Hillert, A.
A1  - Hinton, James Anthony
A1  - Hofmann, W.
A1  - Hofverberg, P.
A1  - Holler, Margitte
A1  - Horns, D.
A1  - Ivascenko, A.
A1  - Jacholkowska, A.
A1  - Jahn, C.
A1  - Jamrozy, M.
A1  - Janiak, M.
A1  - Jankowsky, F.
A1  - Jung-Richardt, I.
A1  - Kastendieck, M. A.
A1  - Katarzynski, K.
A1  - Katz, U.
A1  - Kaufmann, S.
A1  - Khelifi, B.
A1  - Kieffer, M.
A1  - Klepser, S.
A1  - Klochkov, D.
A1  - Kluzniak, W.
A1  - Kolitzus, D.
A1  - Komin, Nu
A1  - Kosack, K.
A1  - Krakau, S.
A1  - Krayzel, F.
A1  - Krueger, P. P.
A1  - Laffon, H.
A1  - Lamanna, G.
A1  - Lefaucheur, J.
A1  - Lefranc, V.
A1  - Lemiere, A.
A1  - Lemoine-Goumard, M.
A1  - Lenain, J. -P.
A1  - Lohse, T.
A1  - Lopatin, A.
A1  - Lu, C. -C.
A1  - Marandon, V.
A1  - Marcowith, A.
A1  - Marx, R.
A1  - Maurin, G.
A1  - Maxted, N.
A1  - Mayer, Michael
A1  - McComb, T. J. L.
A1  - Mehault, J.
A1  - Meintjes, P. J.
A1  - Menzler, U.
A1  - Meyer, M.
A1  - Mitchell, A. M. W.
A1  - Moderski, R.
A1  - Mohamed, M.
A1  - Mora, K.
A1  - Moulin, E.
A1  - Murach, T.
A1  - de Naurois, M.
A1  - Niemiec, J.
A1  - Nolan, S. J.
A1  - Oakes, L.
A1  - Odaka, H.
A1  - Ohm, S.
A1  - Opitz, B.
A1  - Ostrowski, M.
A1  - Oya, I.
A1  - Panter, M.
A1  - Parsons, R. D.
A1  - Arribas, M. Paz
A1  - Pekeur, N. W.
A1  - Pelletier, G.
A1  - Petrucci, P. -O.
A1  - Peyaud, B.
A1  - Pita, S.
A1  - Poon, H.
A1  - Puehlhofer, G.
A1  - Punch, M.
A1  - Quirrenbach, A.
A1  - Raab, S.
A1  - Reichardt, I.
A1  - Reimer, A.
A1  - Reimer, O.
A1  - Renaud, M.
A1  - de los Reyes, R.
A1  - Rieger, F.
A1  - Romoli, C.
A1  - Rosier-Lees, S.
A1  - Rowell, G.
A1  - Rudak, B.
A1  - Rulten, C. B.
A1  - Sahakian, V.
A1  - Salek, D.
A1  - Sanchez, David M.
A1  - Santangelo, A.
A1  - Schlickeiser, R.
A1  - Schuessler, F.
A1  - Schulz, A.
A1  - Schwanke, U.
A1  - Schwarzburg, S.
A1  - Schwemmer, S.
A1  - Sol, H.
A1  - Spanier, F.
A1  - Spengler, G.
A1  - Spies, F.
A1  - Stawarz, L.
A1  - Steenkamp, R.
A1  - Stegmann, Christian
A1  - Stinzing, F.
A1  - Stycz, K.
A1  - Sushch, Iurii
A1  - Tavernet, J. -P.
A1  - Tavernier, T.
A1  - Taylor, A. M.
A1  - Terrier, R.
A1  - Tluczykont, M.
A1  - Trichard, C.
A1  - Valerius, K.
A1  - van Eldik, C.
A1  - van Soelen, B.
A1  - Vasileiadis, G.
A1  - Veh, J.
A1  - Venter, C.
A1  - Viana, A.
A1  - Vincent, P.
A1  - Vink, J.
A1  - Voelk, H. J.
A1  - Volpe, F.
A1  - Vorster, M.
A1  - Vuillaume, T.
A1  - Wagner, S. J.
A1  - Wagner, P.
A1  - Wagner, R. M.
A1  - Ward, M.
A1  - Weidinger, M.
A1  - Weitzel, Q.
A1  - White, R.
A1  - Wierzcholska, A.
A1  - Willmann, P.
A1  - Woernlein, A.
A1  - Wouters, D.
A1  - Yang, R.
A1  - Zabalza, V.
A1  - Zaborov, D.
A1  - Zacharias, M.
A1  - Zdziarski, A. A.
A1  - Zech, Alraune
A1  - Zechlin, H. -S.
T1  - Constraints on an Annihilation Signal from a Core of Constant Dark Matter Density around the Milky Way Center with HESS
JF  - Physical review letters
N2  - An annihilation signal of dark matter is searched for from the central region of the Milky Way. Data acquired in dedicated on-off observations of the Galactic center region with H.E.S.S. are analyzed for this purpose. No significant signal is found in a total of similar to 9 h of on-off observations. Upper limits on the velocity averaged cross section, <sigma upsilon >, for the annihilation of dark matter particles with masses in the range of similar to 300 GeV to similar to 10 TeV are derived. In contrast to previous constraints derived from observations of the Galactic center region, the constraints that are derived here apply also under the assumption of a central core of constant dark matter density around the center of the Galaxy. Values of <sigma upsilon > that are larger than 3 x 10(-24) cm(3)/s are excluded for dark matter particles with masses between similar to 1 and similar to 4 TeV at 95% C.L. if the radius of the central dark matter density core does not exceed 500 pc. This is the strongest constraint that is derived on <sigma upsilon > for annihilating TeV mass dark matter without the assumption of a centrally cusped dark matter density distribution in the search region.
Y1  - 2015
U6  - https://doi.org/10.1103/PhysRevLett.114.081301
SN  - 0031-9007
SN  - 1079-7114
VL  - 114
IS  - 8
PB  - American Physical Society
CY  - College Park
ER  - 
TY  - JOUR
A1  - Becker, Michael
A1  - Neumann, Marko
A1  - Tetzner, Julia
A1  - Böse, Susanne
A1  - Knoppick, Henrike
A1  - Maaz, Kai
A1  - Baumert, Jürgen
A1  - Lehmann, Rainer
T1  - Development? Effects of the transition into academically selective schools
JF  - The journal of educational psychology
N2  - The present study investigates school context effects on psychosocial characteristics (academic self-concept, peer relations, school satisfaction, and school anxiety) of high-achieving and gifted students. Students who did or did not make an early transition from elementary to secondary schools for high-achieving and gifted students in 5th grade in Berlin, Germany, are compared in their psychosocial development. The sample comprises 155 early-entry students who moved to an academically selective secondary school (Gymnasium) and 3,169 regular students who remained in elementary school until the end of 6th grade. Overall, a complex pattern of psychosocial development emerged for all students, with both positive and negative outcomes being observed. Specifically, the transition into academically selective learning environments seemed to come at some cost for psychosocial development. Propensity score matching analysis isolating the effects of selective school intake and the school context effect itself revealed negative contextual effects of early transition to Gymnasium on academic self-concept and school anxiety; additionally, the positive trend in peer relations observed among regular students was not discernible among early-entry students.
KW  - psychosocial development
KW  - transition
KW  - ability grouping
KW  - longitudinal design
KW  - propensity score matching
Y1  - 2014
U6  - https://doi.org/10.1037/a0035425
SN  - 0022-0663
SN  - 1939-2176
VL  - 106
IS  - 2
SP  - 555
EP  - 568
PB  - American Psychological Association
CY  - Washington
ER  - 
TY  - BOOK
A1  - Maaz, Kai
A1  - Baumert, Jürgen
A1  - Neumann, Marko
A1  - Becker, Michael
A1  - Dumont, Hanna
T1  - Die Berliner Schulstrukturreform : Bewertung durch die beteiligten Akteure und Konsequenzen des neuen Übergangsverfahrens von der Grundschule in die weiterführenden Schulen
Y1  - 2013
SN  - 978-3-8309-2946-8
PB  - Waxmann
CY  - Münster
ER  -