Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Lithospheric-scale faults related to oblique subduction are responsible for some of the most hazardous earthquakes reported worldwide. The mega-thrust in the Sunda sector of the Sumatran oblique subduction has been intensively studied, especially after the infamous 2004 Mw 9.1 earthquake, but its onshore kinematic complement within the Sumatran subduction, the transform Sumatran Fault System, has received considerably less attention. In this paper, we apply a combination of analysis of Digital Elevation Models (ASTER GDEM) and field evidence to resolve the kinematics of the leading edge of deformation of the northern sector of the Sumatran Fault System. To this end, we mapped the northernmost tip of Sumatra, including the islands to the northwest, between 4.5°N and 6°N. Here, major topographic highs are related to different faults. Using field evidence and our GDEM structural mapping, we can show that in the area where the fault bifurcates into two fault strands, two independent kinematic regimes evolve, both consistent with the large-scale framework of the Sumatran Fault System. Whereas the eastern branch is a classic Riedel system, the western branch features a fold-and-thrust belt. The latter contractional feature accommodated significant amounts (c. 20%) of shortening of the system in the study area. Our field observations of the tip of the NSFS match a strain pattern with a western contractional domain (Pulau Weh thrust splay) and an eastern extensional domain (Pulau Aceh Riedel system), which are together characteristic of the tip of a propagating strike-slip fault, from a mechanical viewpoint. For the first time, we describe the strain partitioning resulting from the propagation of the NSFS in Sumatra mainland. Our study helps understanding complex kinematics of an evolving strike-slip system, and stresses the importance of field studies in addition to remote sensing and geophysical studies.
ISSN: 0040-1951

hal-01467196
https://hal.archives-ouvertes.fr/hal-01467196
DOI : 10.1016/j.tecto.2016.04.050

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
We propose a new geometric approach to describe the qualitative dynamics of chemical reactions networks. By this method we identify metastable regimes, defined as low dimensional regions of the phase space close to which the dynamics is much slower compared to the rest of the phase space. These metastable regimes depend on the network topology and on the orders of magnitude of the kinetic parameters. Benchmarking of the method on a computational biology model repository suggests that the number of metastable regimes is sub-exponential in the number of variables and equations. The dynamics of the network can be described as a sequence of jumps from one metastable regime to another. We show that a geometrically computed con-nectivity graph restricts the set of possible jumps. We also provide finite state machine (Markov chain) models for such dynamic changes. Applied to signal transduction models, our approach unravels dynamical and functional * corresponding author capacities of signalling pathways, as well as parameters responsible for speci-ficity of the pathway response. In particular, for a model of TGFβ signalling, we find that the ratio of TGFBR2 to TGFBR1 receptors concentrations can be used to discriminate between metastable regimes. Using expression data from the NCI60 panel of human tumor cell lines, we show that aggressive and non-aggressive tumour cell lines function in different metastable regimes and can be distinguished by measuring the relative concentrations of receptors of the two types.
ISSN: 0303-2647

hal-01379033
https://hal.inria.fr/hal-01379033
https://hal.inria.fr/hal-01379033/document
https://hal.inria.fr/hal-01379033/file/Samal_et_al_Biosystems_final.pdf
DOI : 10.1016/j.biosystems.2016.07.004

Éditeur(s) : HAL CCSD IOP Publishing
Résumé : We present the results of an inter-laboratory comparison of EPMA analysis at low voltage (5-6 kV) of three monophasic alloy steel samples. The aim of the work was to obtain an estimate of the present situation of low-voltage analysis of steel and identify needs for improvement. EPMA analyses of the samples were conducted by seven participant groups using electron microprobes and scanning electron microscopes of different kind, equipped with wavelength- and/or energy-dispersive X-ray spectrometers, and employing their own methodology of analysis. The results using WDS showed essentially an underestimation of the Cr contents, with relative deviations from the reference values ranging from -0.7 % to -17 %, and an overestimation of Fe and Ni, with relative deviations from the reference composition ranging from -4 % to +30 %, and from +14 % to +42 %, respectively. The relative deviations obtained by using EDS showed larger scatter, ranging from -16 % to +54 % for Cr, -0.4 % to +66 % for Fe and from +13 % to +90 % for Ni. Reasons for the differences observed and the scatter of results are discussed.
ISSN: 1757-8981

hal-00813999
https://hal.archives-ouvertes.fr/hal-00813999
DOI : 10.1088/1757-899X/32/1/012014

Éditeur(s) : HAL CCSD Wiley-Blackwell
Résumé : International audience
UNLABELLED: Interleukin (IL)-33, a member of the IL-1 cytokine family, positively correlates with acute hepatitis and chronic liver failure in mice and humans. IL-33 is expressed in hepatocytes and is regulated by natural killer T (NKT) cells during concanavalin A (ConA)-induced acute liver injury. Here, we investigated the molecular mechanisms underlying the expression of IL-33 during acute hepatitis. The expression of IL-33 and its regulation by death receptor pathways was investigated after the induction of ConA-acute hepatitis in wildtype (WT), perforin(-/-) , tumor necrosis factor related apoptosis inducing ligand (TRAIL)(-/-) , and NKT cell-deficient (CD1d(-/-) ) mice. In addition, we used a model of acute liver injury by administering Jo2/Fas-antibody or D-galactosamine-tumor necrosis factor alpha (TNFα) in WT mice. Finally, the effect of TRAIL on IL-33 expression was assessed in primary cultured murine hepatocytes. We show that IL-33 expression in hepatocytes is partially controlled by perforin during acute liver injury, but not by TNFα or Fas ligand (FasL). Interestingly, the expression of IL-33 in hepatocytes is blocked during ConA-acute hepatitis in TRAIL-deficient mice compared to WT mice. In contrast, administration of recombinant murine TRAIL associated with ConA-priming in CD1d-deficient mice or in vitro stimulation of murine hepatocytes by TRAIL but not by TNFα or Jo2 induced IL-33 expression in hepatocytes. The IL-33-deficient mice exhibited more severe ConA liver injury than WT controls, suggesting a protective effect of IL-33 in ConA-hepatitis. CONCLUSION: The expression of IL-33 during acute hepatitis is dependent on TRAIL, but not on FasL or TNFα.
ISSN: 0270-9139

hal-00874194
https://hal.archives-ouvertes.fr/hal-00874194
PUBMED : 22961755
DOI : 10.1002/hep.25893