Landslide mapping and monitoring by using radar and optical remote sensing: examples from the EC-FP7 project SAFER

This paper focuses on the Landslide Thematic services of the EU-funded FP7-SPACE project SAFER (Services and Applications For Emergency Response) for inventory mapping, monitoring and rapid mapping by using Earth Observation (EO). We exploited satellite Interferometric Synthetic Aperture Radar (InSAR) and Object-Based Image Analysis (OBIA), and discuss example applications in South Tyrol and Abruzzo (Italy), Lower Austria (Austria), Lubietova (Slovakia) and the Kaohsiung County (Taiwan). These case studies showcase the significance of radar and optical EO data, InSAR and OBIA methods for landslide mapping and monitoring in different geological environments and during all phases of emergency management: mitigation, preparedness, crisis and recovery

C9orf72 arginine-rich dipeptide proteins interact with ribosomal proteins in vivo to induce a toxic translational arrest that is rescued by eIF1A.

A GGGGCC hexanucleotide repeat expansion within the C9orf72 gene is the most common genetic cause of both amyotrophic lateral sclerosis and frontotemporal dementia. Sense and antisense repeat-containing transcripts undergo repeat-associated non-AUG-initiated translation to produce five dipeptide proteins (DPRs). The polyGR and polyPR DPRs are extremely toxic when expressed in Drosophila neurons. To determine the mechanism that mediates this toxicity, we purified DPRs from the Drosophila brain and used mass spectrometry to identify the in vivo neuronal DPR interactome. PolyGR and polyPR interact with ribosomal proteins, and inhibit translation in both human iPSC-derived motor neurons, and adult Drosophila neurons. We next performed a screen of 81 translation-associated proteins in GGGGCC repeat-expressing Drosophila to determine whether this translational repression can be overcome and if this impacts neurodegeneration. Expression of the translation initiation factor eIF1A uniquely rescued DPR-induced toxicity in vivo, indicating that restoring translation is a potential therapeutic strategy. These data directly implicate translational repression in C9orf72 repeat-induced neurodegeneration and identify eIF1A as a novel modifier of C9orf72 repeat toxicity

C9orf72 arginine-rich dipeptide proteins interact with ribosomal proteins in vivo to induce a toxic translational arrest that is rescued by eIF1A

A GGGGCC hexanucleotide repeat expansion within the C9orf72 gene is the most common genetic cause of both amyotrophic lateral sclerosis and frontotemporal dementia. Sense and antisense repeat-containing transcripts undergo repeat-associated non-AUG-initiated translation to produce five dipeptide proteins (DPRs). The polyGR and polyPR DPRs are extremely toxic when expressed in Drosophila neurons. To determine the mechanism that mediates this toxicity, we purified DPRs from the Drosophila brain and used mass spectrometry to identify the in vivo neuronal DPR interactome. PolyGR and polyPR interact with ribosomal proteins, and inhibit translation in both human iPSC-derived motor neurons, and adult Drosophila neurons. We next performed a screen of 81 translation-associated proteins in GGGGCC repeat-expressing Drosophila to determine whether this translational repression can be overcome and if this impacts neurodegeneration. Expression of the translation initiation factor eIF1A uniquely rescued DPR-induced toxicity in vivo, indicating that restoring translation is a potential therapeutic strategy. These data directly implicate translational repression in C9orf72 repeat-induced neurodegeneration and identify eIF1A as a novel modifier of C9orf72 repeat toxicity

Shape of collective flow in highly central Au(150 A MeV)+Au collisions

Using the FOPI facility at GSI, charged particles (1 ≤Z≤6) produced in the Au(150 A MeV)+Au reaction have been measured at laboratory angles 1.20 < Θlab < 300. Highly central collisions have been selected with two criteria, both dealing with the longitudinal and transverse degrees of freedom of the reaction. The relevance of this selection method is supported by QMD calculations which indicate that such criteria are able to select mean impact parameters less than 2 fm. Bias effects introduced by the criteria have been evaluated. The centre-of-mass polar angle distributions of low energy clusters emitted in these central collisions, have been extracted: the intensity ratio deduced for a transverse to longitudinal emission is found to be R= 1.4 −0.4 +0.2 . Model comparisons using QMD are presented. The value of R appears to depend sensitively on the nucleon-nucleon cross section, σnn. Within this model, a value of σ=25+ - 5 mb is derived