Éditeur(s) : American Geophysical Union
Résumé : We present four companion digital models of the age, age uncertainty, spreading rates, and spreading asymmetries of the world's ocean basins as geographic and Mercator grids with 2 arc min resolution. The grids include data from all the major ocean basins as well as detailed reconstructions of back-arc basins. The age, spreading rate, and asymmetry at each grid node are determined by linear interpolation between adjacent seafloor isochrons in the direction of spreading. Ages for ocean floor between the oldest identified magnetic anomalies and continental crust are interpolated by geological estimates of the ages of passive continental margin segments. The age uncertainties for grid cells coinciding with marine magnetic anomaly identifications, observed or rotated to their conjugate ridge flanks, are based on the difference between gridded age and observed age. The uncertainties are also a function of the distance of a given grid cell to the nearest age observation and the proximity to fracture zones or other age discontinuities. Asymmetries in crustal accretion appear to be frequently related to asthenospheric flow from mantle plumes to spreading ridges, resulting in ridge jumps toward hot spots. We also use the new age grid to compute global residual basement depth grids from the difference between observed oceanic basement depth and predicted depth using three alternative age-depth relationships. The new set of grids helps to investigate prominent negative depth anomalies, which may be alternatively related to subducted slab material descending in the mantle or to asthenospheric flow. A combination of our digital grids and the associated relative and absolute plate motion model with seismic tomography and mantle convection model outputs represents a valuable set of tools to investigate geodynamic problems.
Geochemistry Geophysics Geosystems - G3 (1525-2027) (American Geophysical Union), 2008-04 , Vol. 9 , P. NIL_18-NIL_36

Droits : 2008 American Geophysical Union
http://archimer.ifremer.fr/doc/2008/publication-3900.pdf
DOI:10.1029/2007GC001743
http://archimer.ifremer.fr/doc/00000/3900/

Éditeur(s) : HAL CCSD Landes Bioscience
Résumé : International audience
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
Autophagy

hal-00735751
https://hal.archives-ouvertes.fr/hal-00735751
PUBMED : 22966490

Éditeur(s) : HAL CCSD Wiley
Résumé : International audience
An intensive water vapour intercomparison effort, involving airborne and ground-based water vapour lidar systems, was carried out in the framework of the COPS experiment. The main objective of this paper is to provide accurate error estimates for these systems. Comparisons between the ground-based Raman lidar BASIL and the airborne CNRS DIAL (Differential Absorption Lidar) indicate a mean relative bias between the two sensors, calculated with respect to the mean value of −2.13% (−0.034 g kg−1) in the altitude region 0.5-3.5 km, while comparisons between BASIL and the airborne DLR DIAL lead to a mean relative bias of 1.87% (0.018 g kg−1) in this same altitude region. Comparisons between the ground-based UHOH DIAL and the CNRS DIAL indicate a bias of −3.2% (−0.37 × 1022 m−3) in the altitude range 1.5-4.5 km, while comparisons between the UHOH DIAL and the DLR DIAL indicate a bias of 0.83% (0.06 × 1022 m−3) in this same altitude range. Based on the available comparisons between the ground-based Raman lidar BERTHA and the CNRS DIAL, the mean relative bias is found to be −4.37% (−0.123 g kg−1) in the altitude region 0.5-4.5 km. Comparisons between the ground-based IGN Raman lidar and the CNRS DIAL indicate a bias of 3.18% (0.55 g kg−1) in the altitude range from 0.5 to 4.5 km, while comparisons between the CNRS DIAL and DLR DIAL result in a mean relative bias of 3.93% (1.1 × 1022 m−3) in the altitude interval 0.5-4.0 km. Based on the available statistics of comparisons, benefiting from the fact that the CNRS DIAL was able to be compared with all other lidar systems, and putting equal weight on the data reliability of each instrument, overall relative values for BASIL, BERTHA, IGN Raman lidar, UHOH DIAL, DLR DIAL, and CNRS DIAL, with respect to the mean value, are found to be −0.38, −2.60, 4.90, −1.43, −2.23 and 1.72%, respectively.
ISSN: 0035-9009

hal-00572576
https://hal.archives-ouvertes.fr/hal-00572576
DOI : 10.1002/qj.697

Éditeur(s) : HAL CCSD Wiley Open Access
Résumé : International audience
Estetrol (E4) is a natural estrogen with a long half-life produced only by the human fetal liver during pregnancy. The crystal structures of the estrogen receptor α (ERα) ligand-binding domain bound to 17β-estradiol (E2) and E4 are very similar, as well as their capacity to activate the two activation functions AF-1 and AF-2 and to recruit the coactivator SRC3. In vivo administration of high doses of E4 stimulated uterine gene expression, epithelial proliferation, and prevented atheroma, three recognized nuclear ERα actions. However, E4 failed to promote endothelial NO synthase activation and acceleration of endothelial healing, two processes clearly dependent on membrane-initiated steroid signaling (MISS). Furthermore, E4 antagonized E2 MISS-dependent effects in endothelium but also in MCF-7 breast cancer cell line. This profile of ERα activation by E4, uncoupling nuclear and membrane activation, characterizes E4 as a selective ER modulator which could have medical applications that should now be considered further.
ISSN: 1757-4676

hal-01118028
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01118028
PUBMED : 25214462
PUBMEDCENTRAL : PMC4287935
DOI : 10.15252/emmm.201404112