Géographie de l’inondation des marais de la basse-Loire : l’exemple de la crue de l’hiver 2000-2001

Connaître la géographie de l’inondation des marais de la Basse-Loire (notamment ceux de l’estuaire de la Loire, de la Brière et du lac de Grand-Lieu) est fondamental pour en assurer une gestion adéquate. Cependant, on doit tenir compte des profondes modifications de leur hydrologie par les aménagements hydrauliques réalisés depuis le xviiie siècle. À partir de l’exemple de la dernière grande crue, survenue au cours de l’hiver 2000-2001, l’article montre l’apport de la télédétection spatiale (images des satellites Landsat 7 ETM+ et Spot 4) et aérienne pour délimiter les marais inondés et d’en calculer la surface, en corrélation avec les niveaux d’eau relevés à la même période. Le cas de la commune de Trignac illustre l’intérêt de ce type d’étude pour prévenir les risques liés à l’urbanisation. Une comparaison intersaisonnière et interannuelle révèle l’extension de l’inondation permanente en raison de la multiplication des étangs de chasse.A proper knowledge of the geography of flooding of the marshes of the Lower Loire (especially those of the estuary, La Brière and the Lac de Grand-Lieu) is essential to ensure correct management. Nevertheless, we must take into account the considerable changes in the hydrology as a result of the various hydraulic projects carried out since the 18th century. Taking the last major flood, in the winter of 2000-2001, as an example the authors demonstrate how remote sensing – both satellite, using Landsat 7 ETM+ and SPOT 4 images, and aerial – can be used to mark the limits of the marshes flooded and calculate their surface area, in correlation with the water levels registered during the same period. The case of the Commune of Trignac shows the interest of this type of study in preventing threats linked to urban development. An inter-seasonal and inter-annual comparison demonstrates the extent of permanent flooding due to the growing number of ponds created for shooting waterfowl

Non-severe eosinophilic granulomatosis with polyangiitis: long-term outcomes after remission-induction trial

Abstract Objective In a previous controlled trial, 1-year adjunction of AZA to glucocorticoids (GC) for patients with non-severe, newly diagnosed eosinophilic granulomatosis with polyangiitis (EGPA) failed to lower remission failure, vasculitis relapse and isolated asthma/rhinosinus exacerbation rates, or cumulative GC use at month (M) 24. The aim of this study was to analyse longer-term outcomes to determine whether subsequent vasculitis relapse or isolated asthma/rhinosinus exacerbation (IARE) rates differed. Methods After M24, patients were followed prospectively, being treated based on physicians’ best judgment. Flares and reasons for increased GC dose or immunosuppressant use were recorded, and reviewed according to randomization group to distinguish vasculitis relapses from IAREs according to EGPA Task Force recommendations. Results Fifty EGPA trial participants were followed for a median (interquartile range) of 6.3 (5.4–7.6) years; two (4%) died 11 months post-inclusion. By M24, vasculitis had relapsed in 21/49 (43%) patients and 14/50 (28%) had IAREs. Another patient died 4.8 years post-inclusion (infection). Among nine patients with subsequent vasculitis relapses, three had a major relapse and three had their first relapse after M24; among 25 patients with later IAREs, 17 occurred after M24. At 5 years, respective vasculitis relapse and IARE rates were 48% (95% CI 34.0, 62.6) and 56% (95% CI 41.7, 70.8), with no between-arm differences (P = 0.32 and 0.13). No entry clinical or biological parameter was associated with these outcomes during follow-up. Conclusion These results confirmed that 1-year AZA and GC induction obtained good overall survival but no long-term benefit for non-severe EGPA patients. Vasculitis relapses, occurring mostly during the first 2 years, and IAREs, occurring throughout follow-up, require other preventive treatments. Trial registration ClinicalTrials.gov, https://clinicaltrials.gov, NCT00647166. </jats:sec

Adding Azathioprine to Remission-Induction Glucocorticoids for Eosinophilic Granulomatosis With Polyangiitis (Churg-Strauss), Microscopic Polyangiitis, or Polyarteritis Nodosa Without Poor Prognosis Factors

International audienc

A highly virulent variant of HIV-1 circulating in the Netherlands

We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log 10 increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV—CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences—is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence. </jats:p

A highly virulent variant of HIV-1 circulating in the Netherlands

We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log10 increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV-CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences-is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence