TY  - JOUR
A1  - Arridge, Christopher S.
A1  - Achilleos, N.
A1  - Agarwal, Jessica
A1  - Agnor, C. B.
A1  - Ambrosi, R.
A1  - Andre, N.
A1  - Badman, S. V.
A1  - Baines, K.
A1  - Banfield, D.
A1  - Barthelemy, M.
A1  - Bisi, M. M.
A1  - Blum, J.
A1  - Bocanegra-Bahamon, T.
A1  - Bonfond, B.
A1  - Bracken, C.
A1  - Brandt, P.
A1  - Briand, C.
A1  - Briois, C.
A1  - Brooks, S.
A1  - Castillo-Rogez, J.
A1  - Cavalie, T.
A1  - Christophe, B.
A1  - Coates, Andrew J.
A1  - Collinson, G.
A1  - Cooper, J. F.
A1  - Costa-Sitja, M.
A1  - Courtin, R.
A1  - Daglis, I. A.
A1  - De Pater, Imke
A1  - Desai, M.
A1  - Dirkx, D.
A1  - Dougherty, M. K.
A1  - Ebert, R. W.
A1  - Filacchione, Gianrico
A1  - Fletcher, Leigh N.
A1  - Fortney, J.
A1  - Gerth, I.
A1  - Grassi, D.
A1  - Grodent, D.
A1  - Grün, Eberhard
A1  - Gustin, J.
A1  - Hedman, M.
A1  - Helled, R.
A1  - Henri, P.
A1  - Hess, Sebastien
A1  - Hillier, J. K.
A1  - Hofstadter, M. H.
A1  - Holme, R.
A1  - Horanyi, M.
A1  - Hospodarsky, George B.
A1  - Hsu, S.
A1  - Irwin, P.
A1  - Jackman, C. M.
A1  - Karatekin, O.
A1  - Kempf, Sascha
A1  - Khalisi, E.
A1  - Konstantinidis, K.
A1  - Kruger, H.
A1  - Kurth, William S.
A1  - Labrianidis, C.
A1  - Lainey, V.
A1  - Lamy, L. L.
A1  - Laneuville, Matthieu
A1  - Lucchesi, D.
A1  - Luntzer, A.
A1  - MacArthur, J.
A1  - Maier, A.
A1  - Masters, A.
A1  - McKenna-Lawlor, S.
A1  - Melin, H.
A1  - Milillo, A.
A1  - Moragas-Klostermeyer, Georg
A1  - Morschhauser, Achim
A1  - Moses, J. I.
A1  - Mousis, O.
A1  - Nettelmann, N.
A1  - Neubauer, F. M.
A1  - Nordheim, T.
A1  - Noyelles, B.
A1  - Orton, G. S.
A1  - Owens, Mathew
A1  - Peron, R.
A1  - Plainaki, C.
A1  - Postberg, F.
A1  - Rambaux, N.
A1  - Retherford, K.
A1  - Reynaud, Serge
A1  - Roussos, E.
A1  - Russell, C. T.
A1  - Rymer, Am.
A1  - Sallantin, R.
A1  - Sanchez-Lavega, A.
A1  - Santolik, O.
A1  - Saur, J.
A1  - Sayanagi, Km.
A1  - Schenk, P.
A1  - Schubert, J.
A1  - Sergis, N.
A1  - Sittler, E. C.
A1  - Smith, A.
A1  - Spahn, Frank
A1  - Srama, Ralf
A1  - Stallard, T.
A1  - Sterken, V.
A1  - Sternovsky, Zoltan
A1  - Tiscareno, M.
A1  - Tobie, G.
A1  - Tosi, F.
A1  - Trieloff, M.
A1  - Turrini, D.
A1  - Turtle, E. P.
A1  - Vinatier, S.
A1  - Wilson, R.
A1  - Zarkat, P.
T1  - The science case for an orbital mission to Uranus: Exploring the origins and evolution of ice giant planets
JF  - Planetary and space science
N2  - Giant planets helped to shape the conditions we see in the Solar System today and they account for more than 99% of the mass of the Sun's planetary system. They can be subdivided into the Ice Giants (Uranus and Neptune) and the Gas Giants (Jupiter and Saturn), which differ from each other in a number of fundamental ways. Uranus, in particular is the most challenging to our understanding of planetary formation and evolution, with its large obliquity, low self-luminosity, highly asymmetrical internal field, and puzzling internal structure. Uranus also has a rich planetary system consisting of a system of inner natural satellites and complex ring system, five major natural icy satellites, a system of irregular moons with varied dynamical histories, and a highly asymmetrical magnetosphere. Voyager 2 is the only spacecraft to have explored Uranus, with a flyby in 1986, and no mission is currently planned to this enigmatic system. However, a mission to the uranian system would open a new window on the origin and evolution of the Solar System and would provide crucial information on a wide variety of physicochemical processes in our Solar System. These have clear implications for understanding exoplanetary systems. In this paper we describe the science case for an orbital mission to Uranus with an atmospheric entry probe to sample the composition and atmospheric physics in Uranus' atmosphere. The characteristics of such an orbiter and a strawman scientific payload are described and we discuss the technical challenges for such a mission. This paper is based on a white paper submitted to the European Space Agency's call for science themes for its large-class mission programme in 2013.
KW  - Uranus
KW  - Magnetosphere
KW  - Atmosphere
KW  - Natural satellites
KW  - Rings
KW  - Planetary interior
Y1  - 2014
U6  - https://doi.org/10.1016/j.pss.2014.08.009
SN  - 0032-0633
VL  - 104
SP  - 122
EP  - 140
PB  - Elsevier
CY  - Oxford
ER  - 
TY  - JOUR
A1  - Japtok, Lukasz
A1  - Schmitz, Elisabeth I.
A1  - Fayyaz, Susann
A1  - Krämer, Stephanie
A1  - Hsu, Leigh J.
A1  - Kleuser, Burkhard
T1  - Sphingosine 1-phosphate counteracts insulin signaling in pancreatic beta-cells via the sphingosine 1-phosphate receptor subtype 2
JF  - The FASEB journal : the official journal of the Federation of American Societies for Experimental Biology
N2  - Glucolipotoxic stress has been identified as a key player in the progression of pancreatic beta-cell dysfunction contributing to insulin resistance and the development of type 2 diabetes mellitus (T2D). It has been suggested that bioactive lipid intermediates, formed under lipotoxic conditions, are involved in these processes. Here, we show that sphingosine 1-phosphate (S1P) levels are not only increased in palmitate-stimulated pancreatic beta-cells but also regulate beta-cell homeostasis in a divergent manner. Although S1P possesses a prosurvival effect in beta-cells, an enhanced level of the sphingolipid antagonizes insulin-mediated cell growth and survival via the sphingosine 1-phosphate receptor subtype 2 (S1P(2)) followed by an inhibition of Akt-signaling. In an attempt to investigate the role of the S1P/S1P(2) axis in vivo, the New Zealand obese (NZO) diabetic mouse model, characterized by beta-cell loss under high-fat diet (HFD) conditions, was used. The occurrence of T2D was accompanied by an increase of plasma S1P levels. To examine whether S1P contributes to the morphologic changes of islets via S1P(2), the receptor antagonist JTE-013 was administered. Most interestingly, JTE-013 rescued beta-cell damage clearly indicating an important role of the S1P(2) in beta-cell homeostasis. Therefore, the present study provides a new therapeutic strategy to diminish beta-cell dysfunction and the development of T2D.
KW  - type 2 diabetes mellitus
KW  - sphingolipids
KW  - survival
KW  - proliferation
KW  - Akt signaling
Y1  - 2015
U6  - https://doi.org/10.1096/fj.14-263194
SN  - 0892-6638
SN  - 1530-6860
VL  - 29
IS  - 8
SP  - 3357
EP  - 3369
PB  - Federation of American Societies for Experimental Biology
CY  - Bethesda
ER  -