Simulation numérique d'une écoulement au-dessus d'une rampe à l'aide de la méthode des frontières immergées

Nous nous proposons d’étudier numériquement une géométrie étudiée dans le cadre du GDR Contrôle des Décollements, soit une plaque plane avec une rampe descendante, avec ou sans contrôle. Des simulations sont menées en 3D à l’aide d’un code incompressible qui utilise la formulation vitesse-tourbillon des équations de Navier-Stokes. Les écoulements à haute vitesse sont pris en compte à l’aide d’un modèle de sous-maille associée à la Simulation des Grandes Echelles (LES), le modèle d'échelles mixtes. La partie solide de la géométrie est calculée par pénalisation avec une méthode aux frontières immergées. Le maillage est alors cartésien et l’écoulement à l’intérieur du solide imposé à vitesse nulle. Le calcul du vecteur tourbillon aux frontières demande un soin particulier. Le contrôle peut être activé localement à la paroi et mimer les techniques d’aspiration (ou soufflage) ou de jets synthétiques. Nous associons ici dans un nouveau code des techniques présentes au LIMSI dans deux versions de ce code 3D incompressible, soit une version utilisée précédemment à nombres de Reynolds élevés pour simuler des écoulements externes (libres ou autour d’obstacles), avec ou sans contrôle, et une seconde version utilisée pour simuler des écoulements à des nombres de Reynolds plus raisonnables autour d’obstacles calculés par méthode de pénalisation. Un cas proche de la géométrie de référence est modélisé et les premiers essais sont effectués en petit 3D avec et sans contrôle par aspiration. Les objectifs de ce contrôle sont d’une part d’influencer la topologie de la recirculation au niveau de la rampe et d’autre part de réduire la trainée. Par la suite, d'autres cas seront simulés avec des dimensions plus réalistes par rapport à l'expérience de référence et des nombres de Reynolds plus élevés

Best Practices and Pitfalls in Commercializing IVD-Applicable Biomarkers

Before biomarker discoveries can be commercially utilized in clinical laboratories, many studies and surveys need to be completed and many questions answered. Is there a market need? Is there enough scientific and clinical evidence to convince the end users? Is the biomarker patentable? Is the translation into a practical product feasible? Although commercial product development is not the focus of academic research, the route to reach the patients will almost always require a professional commercialization process. Understanding industry and end-user requirements is essential for the successful commercialization of new biomarker assays. The current handbook collects some of the best practices and pitfalls encountered at different phases of biomarker discovery, development, patent protection and technology transfer at universities, hospitals and research organizations. The focus is on in vitro diagnostics (IVD)-applicable biomarkers, i.e. markers intended to provide information on the health status of a person. The input for the collection has been sought from true-life practices: practices found in literature or taught by experts in the field; opinions and expertise of different stakeholders (end users, companies, technology transfer professionals, researchers, financiers); recommendations, regulation and laws; as well as practices learned the hard way, i.e. repeatedly failing somewhere in the process and later adapting the process for increased success. The main target group of the handbook comprises professionals working in Technology Transfer Offices (TTOs). The presented practices are yet not intended to be interpreted as strict rules but rather as a source of inspiration. Optimal ways to proceed with patenting and commercialization significantly vary between cases and circumstances.The handbook has been prepared within the EU-project Biomarker Commercialization (BIC) comprising 9 partners in the Baltic Sea Region (BSR) united with the same challenges, as well as the common objective of more efficiently bringing new and better IVD-applicable biomarkers from discovery into clinical use. The project's budget is EUR 2.55 million and is co-financed by the European Regional Development Fund through the Interreg Baltic Sea Region Programme with EUR 1.96 million

Opposite effects of statins on mitochondria of cardiac and skeletal muscles: a ‘mitohormesis' mechanism involving reactive oxygen species and PGC-1

Aims Statins protect against cardiovascular-related mortality but induce skeletal muscle toxicity. To investigate mechanisms of statins, we tested the hypothesis that statins optimized cardiac mitochondrial function but impaired vulnerable skeletal muscle by inducing different level of reactive oxygen species (ROS). Methods and results In atrium of patients treated with statins, ROS production was decreased and oxidative capacities were enhanced together with an extensive augmentation of mRNAs expression of peroxisome proliferator-activated receptor gamma co-activator (PGC-1) family. However, in deltoid biopsies from patients with statin-induced muscular myopathy, oxidative capacities were decreased together with ROS increase and a collapse of PGC-1 mRNA expression. Several animal and cell culture experiments were conducted and showed by using ROS scavengers that ROS production was the triggering factor responsible of atorvastatin-induced activation of mitochondrial biogenesis pathway and improvement of antioxidant capacities in heart. Conversely, in skeletal muscle, the large augmentation of ROS production following treatment induced mitochondrial impairments, and reduced mitochondrial biogenesis mechanisms. Quercetin, an antioxidant molecule, was able to counteract skeletal muscle deleterious effects of atorvastatin in rat. Conclusion Our findings identify statins as a new activating factor of cardiac mitochondrial biogenesis and antioxidant capacities, and suggest the importance of ROS/PGC-1 signalling pathway as a key element in regulation of mitochondrial function in cardiac as well as skeletal muscle

Comparison of Atmospheric and Lithospheric Culturable Bacterial Communities from Two Dissimilar Active Volcanic Sites, Surtsey Island and Fimmvörðuháls Mountain in Iceland

This research was funded by the Icelandic Research fund (IRF, RANNÍS) (174425-051). T.Š.-T. was supported by The Danish National Research Foundation (DNRF106, to the Stellar Astrophysics Centre, Aarhus University), the AUFF Nova programme (AUFF-E-2015-FLS-9-10), the Novo Nordisk Foundation (NNF19OC0056963) and the Villum Fonden (23175 and 37435). The Europlanet 2020 Research Infrastructure TA program (18-EPN4-059) funded T.Š.-T. participation in the sampling campaign.Surface microbes are aerosolized into the atmosphere by wind and events such as dust storms and volcanic eruptions. Before they reach their deposition site, they experience stressful atmospheric conditions which preclude the successful dispersal of a large fraction of cells. In this study, our objectives were to assess and compare the atmospheric and lithospheric bacterial cultivable diversity of two geographically different Icelandic volcanic sites: the island Surtsey and the Fimmvörðuháls mountain, to predict the origin of the culturable microbes from these sites, and to select airborne candidates for further investigation. Using a combination of MALDI Biotyper analysis and partial 16S rRNA gene sequencing, a total of 1162 strains were identified, belonging to 72 species affiliated to 40 genera with potentially 26 new species. The most prevalent phyla identified were Proteobacteria and Actinobacteria. Statistical analysis showed significant differences between atmospheric and lithospheric microbial communities, with distinct communities in Surtsey’s air. By combining the air mass back trajectories and the analysis of the closest representative species of our isolates, we concluded that 85% of our isolates came from the surrounding environments and only 15% from long distances. The taxonomic proportions of the isolates were reflected by the site’s nature and location.Peer reviewe

Opposite effects of statins on mitochondria of cardiac and skeletal muscles: a 'mitohormesis' mechanism involving reactive oxygen species and PGC-1

Aims Statins protect against cardiovascular-related mortality but induce skeletal muscle toxicity. To investigate mechanisms of statins, we tested the hypothesis that statins optimized cardiac mitochondrial function but impaired vulnerable skeletal muscle by inducing different level of reactive oxygen species (ROS). Methods and results In atrium of patients treated with statins, ROS production was decreased and oxidative capacities were enhanced together with an extensive augmentation of mRNAs expression of peroxisome proliferator-activated receptor gamma co-activator (PGC-1) family. However, in deltoid biopsies from patients with statin-induced muscular myopathy, oxidative capacities were decreased together with ROS increase and a collapse of PGC-1 mRNA expression. Several animal and cell culture experiments were conducted and showed by using ROS scavengers that ROS production was the triggering factor responsible of atorvastatin-induced activation of mitochondrial biogenesis pathway and improvement of antioxidant capacities in heart. Conversely, in skeletal muscle, the large augmentation of ROS production following treatment induced mitochondrial impairments, and reduced mitochondrial biogenesis mechanisms. Quercetin, an antioxidant molecule, was able to counteract skeletal muscle deleterious effects of atorvastatin in rat. Conclusion Our findings identify statins as a new activating factor of cardiac mitochondrial biogenesis and antioxidant capacities, and suggest the importance of ROS/PGC-1 signalling pathway as a key element in regulation of mitochondrial function in cardiac as well as skeletal muscles

Effects of self-paced interval and continuous training on health markers in women

This is the final version of the article. Available from Springer Verlag via the DOI in this record.PURPOSE: To compare the effects of self-paced high-intensity interval and continuous cycle training on health markers in premenopausal women. METHODS: Forty-five inactive females were randomised to a high-intensity interval training (HIIT; n = 15), continuous training (CT; n = 15) or an inactive control (CON; n = 15) group. HIIT performed 5 × 5 min sets comprising repetitions of 30-s low-, 20-s moderate- and 10-s high-intensity cycling with 2 min rest between sets. CT completed 50 min of continuous cycling. Training was completed self-paced, 3 times weekly for 12 weeks. RESULTS: Peak oxygen uptake (16 ± 8 and 21 ± 12%), resting heart rate (HR) (-5 ± 9 and -4 ± 7 bpm) and visual and verbal learning improved following HIIT and CT compared to CON (P  0.05). No outcome variable changed in the CON group (P > 0.05). CONCLUSIONS: Twelve weeks of self-paced HIIT and CT were similarly effective at improving cardiorespiratory fitness, resting HR and cognitive function in inactive premenopausal women, whereas blood pressure, submaximal HR, well-being and body mass adaptations were training-type-specific. Both training methods improved established health markers, but the adaptations to HIIT were evoked for a lower time commitment.The study was supported by FIFA-Medical Assessment and Research Centre (F-MARC)

The physiological impact of high?intensity interval training in octogenarians with comorbidities

BackgroundDeclines in cardiorespiratory fitness (CRF) and fat-free mass (FFM) with age are linked to mortality, morbidity and poor quality of life. High-intensity interval training (HIIT) has been shown to improve CRF and FFM in many groups, but its efficacy in the very old, in whom comorbidities are present is undefined. We aimed to assess the efficacy of and physiological/metabolic responses to HIIT, in a cohort of octogenarians with comorbidities (e.g. hypertension and osteoarthritis).MethodsTwenty-eight volunteers (18 men, 10 women, 81.2 ± 0.6 years, 27.1 ± 0.6 kg·m−2) with American Society of Anaesthesiology (ASA) Grade 2–3 status each completed 4 weeks (12 sessions) HIIT after a control period of equal duration. Before and after each 4 week period, subjects underwent body composition assessments and cardiopulmonary exercise testing. Quadriceps muscle biopsies (m. vastus lateralis) were taken to quantify anabolic signalling, mitochondrial oxidative phosphorylation, and cumulative muscle protein synthesis (MPS) over 4-weeks.ResultsIn comorbid octogenarians, HIIT elicited improvements in CRF (anaerobic threshold: +1.2 ± 0.4 ml·kg−1·min−1, P = 0.001). HIIT also augmented total FFM (47.2 ± 1.4 to 47.6 ± 1.3 kg, P = 0.04), while decreasing total fat mass (24.8 ± 1.3 to 24 ± 1.2 kg, P = 0.0002) and body fat percentage (33.1 ± 1.5 to 32.1 ± 1.4%, P = 0.0008). Mechanistically, mitochondrial oxidative phosphorylation capacity increased after HIIT (i.e. citrate synthase activity: 52.4 ± 4 to 67.9 ± 5.1 nmol·min−1·mg−1, P = 0.005; membrane protein complexes (C): C-II, 1.4-fold increase, P = 0.002; C-III, 1.2-fold increase, P = 0.03), as did rates of MPS (1.3 ± 0.1 to 1.5 ± 0.1%·day−1, P = 0.03). The increase in MPS was supported by up-regulated phosphorylation of anabolic signalling proteins (e.g. AKT, p70S6K, and 4E-BP1; all P < 0.05). There were no changes in any of these parameters during the control period. No adverse events were reported throughout the study.ConclusionsThe HIIT enhances skeletal muscle mass and CRF in octogenarians with disease, with up-regulation of MPS and mitochondrial capacity likely underlying these improvements. HIIT can be safely delivered to octogenarians with disease and is an effective, time-efficient intervention to improve muscle mass and physical function in a short time frame