Sea state and rain: a second take on dual-frequency altimetry

TOPEX and Jason were the first two dual-frequency altimeters in space, with both operating at Ku- and C-band. Each thus gives two measurements of the normalized backscatter, sigma0, (from which wind speed is calculated) and two estimates of wave height. Departures from a well-defined relationship between the Ku- and C-band sigma0 values give an indication of rain.This paper investigates differences between the two instruments using data from Jason's verification phase. Jason's Ku-band estimates of wave height are ~1.8% less than TOPEX's, whereas its sigma0 values are higher. When these effects have been removed the root mean square (r.m.s.) mismatch between TOPEX and Jason's Ku-band observations is close to that for TOPEX's observations at its two frequencies, and the changes in sigma0 with varying wave height conditions are the same for the two altimeters. Rain flagging and quantitative estimates of rain rate are both based on the atmospheric attenuation derived from the sigma0 measurements at the two frequencies. The attenuation estimates of TOPEX and Jason agree very well, and a threshold of -0.5 dB is effective at removing the majority of spurious data records from the Jason GDRs. In the high sigma0 regime, anomalous data can be cause by processes other than rain. Consequently, for these low wind conditions, neither can reliable rain detection be based on altimetry alone, nor can a generic rain flag be expected to remove all suspect data

PharOS, a multicore OS ready for safety-related automotive systems: results and future prospects

International audienceAutomotive electrical/electronic architectures need to perform more and more functions that are mapped onto many different electronic control units (ECU) because of their different safety levels or different application domains (body, powertrain, multimedia, etc.). Freedom of interference is required to comply with the upcoming ISO 26262 standard for mixing different ASIL levels on the same ECU and is also required to cope with the safe integration of software from different suppliers. PharOS provides dedicated software partitioning mechanisms as well as controlled and efficient resource sharing by construction, from the design to the implementation stages. The main features of PharOS, contributing to this property, are presented in this paper as well as the results on its application an industry-driven case study and associated future prospects

Role of Interleukin 17 in arthritis chronicity through survival of synoviocytes via regulation of synoviolin expression

Background: The use of TNF inhibitors has been a major progress in the treatment of chronic inflammation. However, not all patients respond. In addition, response will be often lost when treatment is stopped. These clinical aspects indicate that other cytokines might be involved and we focus here on the role of IL-17. In addition, the chronic nature of joint inflammation may contribute to reduced response and enhanced chronicity. Therefore we studied the capacity of IL-17 to regulate synoviolin, an E3 ubiquitin ligase implicated in synovial hyperplasia in human rheumatoid arthritis (RA) FLS and in chronic reactivated streptococcal cell wall (SCW)-induced arthritis.<p></p> Methodology/Principal Findings: Chronic reactivated SCW-induced arthritis was examined in IL-17R deficient and wild-type mice. Synoviolin expression was analysed by real-time RT-PCR, Western Blot or immunostaining in RA FLS and tissue, and p53 assessed by Western Blot. Apoptosis was detected by annexin V/propidium iodide staining, SS DNA apoptosis ELISA kit or TUNEL staining and proliferation by PCNA staining. IL-17 receptor A (IL-17RA), IL-17 receptor C (IL-17-RC) or synoviolin inhibition were achieved by small interfering RNA (siRNA) or neutralizing antibodies. IL-17 induced sustained synoviolin expression in RA FLS. Sodium nitroprusside (SNP)-induced RA FLS apoptosis was associated with reduced synoviolin expression and was rescued by IL-17 treatment with a corresponding increase in synoviolin expression. IL-17RC or IL-17RA RNA interference increased SNP-induced apoptosis, and decreased IL-17-induced synoviolin. IL-17 rescued RA FLS from apoptosis induced by synoviolin knockdown. IL-17 and TNF had additive effects on synoviolin expression and protection against apoptosis induced by synoviolin knowndown. In IL-17R deficient mice, a decrease in arthritis severity was characterized by increased synovial apoptosis, reduced proliferation and a marked reduction in synoviolin expression. A distinct absence of synoviolin expressing germinal centres in IL-17R deficient mice contrasted with synoviolin positive B cells and Th17 cells in synovial germinal centre-like structures.<p></p> Conclusion/Significance: IL-17 induction of synoviolin may contribute at least in part to RA chronicity by prolonging the survival of RA FLS and immune cells in germinal centre reactions. These results extend the role of IL-17 to synovial hyperplasia.<p></p&gt

Antarctic icebergs: A significant natural ocean sound source in the Southern Hemisphere

In late 2007, two massive icebergs, C19a and B15a, drifted into open water and slowly disintegrated in the southernmost Pacific Ocean. Archived acoustic records show that the high-intensity underwater sounds accompanying this breakup increased ocean noise levels at mid-to-equatorial latitudes over a period of ~1.5 years. More typically, seasonal variations in ocean noise, which are characterized by austral summer-highs and winter-lows, appear to be modulated by the annual cycle of Antarctic iceberg drift and subsequent disintegration. This seasonal pattern is observed in all three Oceans of the Southern Hemisphere. The life cycle of Antarctic icebergs affects not only marine ecosystem but also the sound environment in far-reaching areas and must be accounted for in any effort to isolate anthropogenic or climate-induced noise contributions to the ocean soundscape.Keywords: Trend, Seasonality, Antarctica, Ocean noise, Iceber

In Antisynthetase Syndrome, ACPA Are Associated With Severe and Erosive Arthritis: An Overlapping Rheumatoid Arthritis and Antisynthetase Syndrome

International audienceAbstract: Anticitrullinated peptide/protein antibodies (ACPA), which are highly specific for rheumatoid arthritis (RA), may be found in some patients with other systemic autoimmune diseases. The clinical significance of ACPA in patients with antisynthetase syndrome (ASS), a systemic disease characterized by the association of myositis, interstitial lung disease, polyarthralgia, and/or polyarthritis, has not yet been evaluated with regard to phenotype, prognosis, and response to treatment. ACPA-positive ASS patients were first identified among a French multicenter registry of patients with ASS. Additionally, all French rheumatology and internal medicine practitioners registered on the Club Rhumatismes et Inflammation web site were asked to report their observations of ASS patients with ACPA. The 17 collected patients were retrospectively studied using a standardized questionnaire and compared with 34 unselected ACPA-negative ASS patients in a case–control study. All ACPA-positive ASS patients suffered from arthritis versus 41% in the control group (P 7-year mean follow-up, extra-articular outcomes and survival were not different. ACPA-positive ASS patients showed an overlapping RA–ASS syndrome, were at high risk of refractory erosive arthritis, and might experience ASS flare when treated with antitumor necrosis factor drugs. In contrast, other biologics such as anti-CD20 mAb were effective in this context, without worsening systemic involvements

Bcl-2 Inhibits the Innate Immune Response during Early Pathogenesis of Murine Congenital Muscular Dystrophy

Laminin α2 (LAMA2)-deficient congenital muscular dystrophy is a severe, early-onset disease caused by abnormal levels of laminin 211 in the basal lamina leading to muscle weakness, transient inflammation, muscle degeneration and impaired mobility. In a Lama2-deficient mouse model for this disease, animal survival is improved by muscle-specific expression of the apoptosis inhibitor Bcl-2, conferred by a MyoD-hBcl-2 transgene. Here we investigated early disease stages in this model to determine initial pathological events and effects of Bcl-2 on their progression. Using quantitative immunohistological and mRNA analyses we show that inflammation occurs very early in Lama2-deficient muscle, some aspects of which are reduced or delayed by the MyoD-hBcl-2 transgene. mRNAs for innate immune response regulators, including multiple Toll-like receptors (TLRs) and the inflammasome component NLRP3, are elevated in diseased muscle compared with age-matched controls expressing Lama2. MyoD-hBcl-2 inhibits induction of TLR4, TLR6, TLR7, TLR8 and TLR9 in Lama2-deficient muscle compared with non-transgenic controls, and leads to reduced infiltration of eosinophils, which are key death effector cells. This congenital disease model provides a new paradigm for investigating cell death mechanisms during early stages of pathogenesis, demonstrating that interactions exist between Bcl-2, a multifunctional regulator of cell survival, and the innate immune response

Different Molecular Signatures in Magnetic Resonance Imaging-Staged Facioscapulohumeral Muscular Dystrophy Muscles

Facioscapulohumeral muscular dystrophy (FSHD) is one of the most common muscular dystrophies and is characterized by a non-conventional genetic mechanism activated by pathogenic D4Z4 repeat contractions. By muscle Magnetic Resonance Imaging (MRI) we observed that T2-short tau inversion recovery (T2-STIR) sequences identify two different conditions in which each muscle can be found before the irreversible dystrophic alteration, marked as T1-weighted sequence hyperintensity, takes place. We studied these conditions in order to obtain further information on the molecular mechanisms involved in the selective wasting of single muscles or muscle groups in this disease