Project factsheet for EC DG RTD brochure

The European Commission DG Research brochure contains project factsheets for FP7 funded Integrated Activities projects. Each factsheet is one page (recto-verso) detailing the general aims and scope of the project. The factsheets are directed at the general public

EuCARD Newsletter Issue 1

European Coordination for Accelerator Research and Development (EuCARD) Newsletter Issue 1: April - June 2009 * A word from the Coordinator * EuCARD in a nutshell * The EuCARD website * MICE - see how they run * For EuCARD members: FAQ

EuCARD Newsletter Issue 3

European Coordination for Accelerator Research and Development (EuCARD) Newsletter Issue 3: October - December 2009 * A word on behalf of the Steering Committee * Cryocatcher in the GSI * Strategy and the Spallation Source * Accelerators for hadron therapy * For EuCARD members: publication

FAS-dependent cell death in α-synuclein transgenic oligodendrocyte models of multiple system atrophy

Multiple system atrophy is a parkinsonian neurodegenerative disorder. It is cytopathologically characterized by accumulation of the protein p25α in cell bodies of oligodendrocytes followed by accumulation of aggregated α-synuclein in so-called glial cytoplasmic inclusions. p25α is a stimulator of α-synuclein aggregation, and coexpression of α-synuclein and p25α in the oligodendroglial OLN-t40-AS cell line causes α-synuclein aggregate-dependent toxicity. In this study, we investigated whether the FAS system is involved in α-synuclein aggregate dependent degeneration in oligodendrocytes and may play a role in multiple system atrophy. Using rat oligodendroglial OLN-t40-AS cells we demonstrate that the cytotoxicity caused by coexpressing α-synuclein and p25α relies on stimulation of the death domain receptor FAS and caspase-8 activation. Using primary oligodendrocytes derived from PLP-α-synuclein transgenic mice we demonstrate that they exist in a sensitized state expressing pro-apoptotic FAS receptor, which makes them sensitive to FAS ligand-mediated apoptosis. Immunoblot analysis shows an increase in FAS in brain extracts from multiple system atrophy cases. Immunohistochemical analysis demonstrated enhanced FAS expression in multiple system atrophy brains notably in oligodendrocytes harboring the earliest stages of glial cytoplasmic inclusion formation. Oligodendroglial FAS expression is an early hallmark of oligodendroglial pathology in multiple system atrophy that mechanistically may be coupled to α-synuclein dependent degeneration and thus represent a potential target for protective intervention

EuCARD Newsletter Issue 2

European Coordination for Accelerator Research and Development (EuCARD) Newsletter Issue 2: July - September 2009 * A word from the Governing Board Chairman * Amassing the neutrino community * Start by probing the crab cavities * Breaking news for Proton "Surfatrons" * For EuCARD members: Interim reportin

ORBIT PRECISION ANALYSIS OF SMALL MAN-MADE SPACE OBJECTS IN LEO BASED ON RADAR TRACKING MEASUREMENTS

Abstract: The German Space Operations Center (GSOC

Spintronic magnetic anisotropy

An attractive feature of magnetic adatoms and molecules for nanoscale applications is their superparamagnetism, the preferred alignment of their spin along an easy axis preventing undesired spin reversal. The underlying magnetic anisotropy barrier --a quadrupolar energy splitting-- is internally generated by spin-orbit interaction and can nowadays be probed by electronic transport. Here we predict that in a much broader class of quantum-dot systems with spin larger than one-half, superparamagnetism may arise without spin-orbit interaction: by attaching ferromagnets a spintronic exchange field of quadrupolar nature is generated locally. It can be observed in conductance measurements and surprisingly leads to enhanced spin filtering even in a state with zero average spin. Analogously to the spintronic dipolar exchange field, responsible for a local spin torque, the effect is susceptible to electric control and increases with tunnel coupling as well as with spin polarization.Comment: 6 pages with 4 figures + 26 pages of Supplementary Informatio

Observations of the geology and geomorphology of the 1999 Marsokhod test site

The Marsokhod rover returned data from six stations that were used to decipher the geomorphology and geology of a region not previously visited by members of the geomorphology field team. Satellite images and simulated descent images provided information about the regional setting. The landing zone was on an alluvial apron flanking a mountain block to the west and playa surface to the east. Rover color images, infrared spectra analysis of the mountains, and the apron surface provided insight into the rock composition of the nearby mountains. From the return data the geomorphology team interpreted the region to consist of compressionally deformed, ancient marine sediments and igneous rocks exposed by more recent extensional tectonics. Unconsolidated alluvial materials blanket the lower flanks of the mountains. An ancient shoreline cut into alluvial material marks a high stand of water during a past, wetter climate period. Playa sediments floor a present-day, seasonally, dry lake. Observations made by the rover using panoramic and close-up (hand specimens—scale) image data and color scene data confirmed the presence of boulders, cobbles, and fines of various provinces. Rover traverses to sites identified as geologically distinct, such as a fan, channel, shoreline, and playa, provided useful clues to the geologic interpretations. Analysis of local rocks was given context only through comparison with distant geologic features. These results demonstrated the importance of a multifaceted approach to site interpretation through comparison of interpretations derived by differing geologic techniques

Performance of the QWIP Focal Plane Arrays for NASA's Landsat Data Continuity Mission

The focal plane assembly for the Thermal Infrared Sensor (TIRS) instrument on NASA's Landsat Data Continuity Mission (LDCM) consists of three 512 x 640 GaAs Quantum Well Infrared Photodetector (QWIP) arrays. The three arrays are precisely mounted and aligned on a silicon carrier substrate to provide a continuous viewing swath of 1850 pixels in two spectral bands defined by filters placed in close proximity to the detector surfaces. The QWIP arrays are hybridized to Indigo ISC9803 readout integrated circuits (ROICs). QWIP arrays were evaluated from four laboratories; QmagiQ, (Nashua, NH), Army Research Laboratory, (Adelphi, MD}, NASA/ Goddard Space Flight Center, (Greenbelt, MD) and Thales, (Palaiseau, France). All were found to be suitable. The final discriminating parameter was the spectral uniformity of individual pixels relative to each other. The performance of the QWIP arrays and the fully assembled, NASA flight-qualified, focal plane assembly will be reviewed. An overview of the focal plane assembly including the construction and test requirements of the focal plane will also be described

Mouse nuclear myosin I knock-out shows interchangeability and redundancy of myosin isoforms in the cell nucleus.

Nuclear myosin I (NM1) is a nuclear isoform of the well-known "cytoplasmic" Myosin 1c protein (Myo1c). Located on the 11(th) chromosome in mice, NM1 results from an alternative start of transcription of the Myo1c gene adding an extra 16 amino acids at the N-terminus. Previous studies revealed its roles in RNA Polymerase I and RNA Polymerase II transcription, chromatin remodeling, and chromosomal movements. Its nuclear localization signal is localized in the middle of the molecule and therefore directs both Myosin 1c isoforms to the nucleus. In order to trace specific functions of the NM1 isoform, we generated mice lacking the NM1 start codon without affecting the cytoplasmic Myo1c protein. Mutant mice were analyzed in a comprehensive phenotypic screen in cooperation with the German Mouse Clinic. Strikingly, no obvious phenotype related to previously described functions has been observed. However, we found minor changes in bone mineral density and the number and size of red blood cells in knock-out mice, which are most probably not related to previously described functions of NM1 in the nucleus. In Myo1c/NM1 depleted U2OS cells, the level of Pol I transcription was restored by overexpression of shRNA-resistant mouse Myo1c. Moreover, we found Myo1c interacting with Pol II. The ratio between Myo1c and NM1 proteins were similar in the nucleus and deletion of NM1 did not cause any compensatory overexpression of Myo1c protein. We observed that Myo1c can replace NM1 in its nuclear functions. Amount of both proteins is nearly equal and NM1 knock-out does not cause any compensatory overexpression of Myo1c. We therefore suggest that both isoforms can substitute each other in nuclear processes