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- 2019
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Tidskriftsartikel (refereegranskat)
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- Pajola, M., et al.
(författare)
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The Agilkia boulders/pebbles size-frequency distributions : OSIRIS and ROLIS joint observations of 67P surface
- 2016
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Ingår i: Monthly notices of the Royal Astronomical Society. - : Oxford University Press (OUP). - 0035-8711 .- 1365-2966. ; 462, s. S242-S252
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Tidskriftsartikel (refereegranskat)abstract
- By using the images acquired by the OSIRIS (Optical, Spectroscopic and Infrared Remote Imaging System) and ROLIS (ROsetta Lander Imaging System) cameras, we derive the size-frequency distribution (SFD) of cometary pebbles and boulders covering the size range 0.05-30.0 m on the Agilkia landing site. The global SFD measured on OSIRIS images, reflects the different properties of the multiple morphological units present on Agilkia, combined with selection effects related to lifting, transport and redeposition. Contrarily, the different ROLIS SFD derived on the smooth and rough units may be related to their different regolith thickness present on Agilkia. In the thicker, smoother layer, ROLIS mainly measures the SFD of the airfall population which almost completely obliterates the signature of underlying boulders up to a size of the order of 1 m. This is well matched by the power-law index derived analysing coma particles identified by the grain analyser Grain Impact Analyser and Dust Accumulator. This result confirms the important blanketing dynamism of Agilkia. The steeper SFD observed in rough terrains from 0.4 to 2 m could point out intrinsic differences between northern and southern dust size distributions, or it may suggest that the underlying boulders 'peek through' the thinner airfall layer in the rough terrain, thereby producing the observed excess in the decimetre size range. Eventually, the OSIRIS SFD performed on the Philae landing unit may be due to water sublimation from a static population of boulders, affecting smaller boulders before the bigger ones, thus shallowing the original SFD.
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| 3. |
- Bernal, Ivan, 1984, et al.
(författare)
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Exciton broadening and band renormalization due to Dexter-like intervalley coupling
- 2018
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Ingår i: 2D Materials. - : IOP Publishing. - 2053-1583. ; 5:2
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Tidskriftsartikel (refereegranskat)abstract
- A remarkable property of atomically thin transition metal dichalcogenides (TMDs) is the possibility to selectively address single valleys by circularly polarized light. In the context of technological applications, it is very important to understand possible intervalley coupling mechanisms. Here, we show how the Dexter-like intervalley coupling mixes A and B states from opposite valleys leading to a significant broadening γB 1s of the B 1s exciton. The effect is much more pronounced in tungsten-based TMDs, where the coupling excitonic states are quasi-resonant. We calculate a ratio γB B 1s /γA B 1s ≈ 4.0, which is in good agreement with the experimentally measured value of 3.9 ± 0.7. In addition to the broadening effect, the Dexter-like intervalley coupling also leads to a considerable energy renormalization resulting in an increased energetic distance between A 1s and B 1s states.
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| 4. |
- Helferich, Anika M., et al.
(författare)
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Dysregulation of a novel miR-1825/TBCB/TUBA4A pathway in sporadic and familial ALS
- 2018
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Ingår i: Cellular and Molecular Life Sciences (CMLS). - : Springer. - 1420-682X .- 1420-9071. ; 75:23, s. 4301-4319
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Tidskriftsartikel (refereegranskat)abstract
- Genetic and functional studies suggest diverse pathways being affected in the neurodegenerative disease amyotrophic lateral sclerosis (ALS), while knowledge about converging disease mechanisms is rare. We detected a downregulation of microRNA-1825 in CNS and extra-CNS system organs of both sporadic (sALS) and familial ALS (fALS) patients. Combined transcriptomic and proteomic analysis revealed that reduced levels of microRNA-1825 caused a translational upregulation of tubulin-folding cofactor b (TBCB). Moreover, we found that excess TBCB led to depolymerization and degradation of tubulin alpha-4A (TUBA4A), which is encoded by a known ALS gene. Importantly, the increase in TBCB and reduction of TUBA4A protein was confirmed in brain cortex tissue of fALS and sALS patients, and led to motor axon defects in an in vivo model. Our discovery of a microRNA-1825/TBCB/TUBA4A pathway reveals a putative pathogenic cascade in both fALS and sALS extending the relevance of TUBA4A to a large proportion of ALS cases.
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