Walther G.,University of Avignon
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2015
OBJECTIVES—: The first objective of this study was to demonstrate differences within endothelial-dependent and endothelial-independent vasoreactivity in macro- and microcirculation beds among patients with metabolic syndrome (MetS) with and without type 2 diabetes mellitus (T2D) compared with healthy counterparts. The second objective was to determine relationships among the function of macro- and microvascular systems and abdominal adiposity, as well as inflammatory markers in the 3 groups.APPROACH AND RESULTS—: Cross-sectional analyses of 53 patients with MetS without T2D and 25 with T2D, as well as aged 40 years and sex-matched healthy controls included microvascular (cutaneous blood flow measured with laser Doppler flowmetry in response to iontophoresis of acetylcholine and sodium nitroprusside), and macrovascular reactivity (flow-mediated dilation and nitrate-mediated dilation) along with anthropometric measures, plasma glucose, and insulin and inflammatory markers. Compared with controls, MetS participants showed depressed endothelial function of both micro- and macrocirculation beds. T2D in patients with MetS revealed an exacerbated vascular smooth muscle dysfunction in micro- and macrocirculation compared with MetS without T2D. Indices of micro- and macrocirculation were predominantly inversely related to abdominal fat and inflammatory markers.CONCLUSIONS—: MetS was associated with endothelial-dependent and endothelial-independent dysfunction, affecting both the macro- and the microvascular systems. Participants with diabetes mellitus demonstrated the most severe smooth muscle dysfunction. The presence of central abdominal fat and systemic inflammation seems implicated in the pathogenesis of vascular dysfunctions in MetS. © 2015 American Heart Association, Inc.
Szostak J.,University of Lausanne |
Laurant P.,University of Avignon
Clinical Science | Year: 2011
Humans are not programmed to be inactive. The combination of both accelerated sedentary lifestyle and constant food availability disturbs ancient metabolic processes leading to excessive storage of energy in tissue, dyslipidaemia and insulin resistance. As a consequence, the prevalence of Type 2 diabetes, obesity and the metabolic syndrome has increased significantly over the last 30 years. A low level of physical activity and decreased daily energy expenditure contribute to the increased risk of cardiovascular morbidity and mortality following atherosclerotic vascular damage. Physical inactivity leads to the accumulation of visceral fat and consequently the activation of the oxidative stress/inflammation cascade, which promotes the development of atherosclerosis. Considering physical activity as a 'natural' programmed state, it is assumed that it possesses atheroprotective properties. Exercise prevents plaque development and induces the regression of coronary stenosis. Furthermore, experimental studies have revealed that exercise prevents the conversion of plaques into a vulnerable phenotype, thus preventing the appearance of fatal lesions. Exercise promotes atheroprotection possibly by reducing or preventing oxidative stress and inflammation through at least two distinct pathways. Exercise, through laminar shear stress activation, down-regulates endothelial AT1R (angiotensin II type 1 receptor) expression, leading to decreases in NADPH oxidase activity and superoxide anion production, which in turn decreases ROS (reactive oxygen species) generation, and preserves endothelial NO bioavailability and its protective anti-atherogenic effects. Contracting skeletal muscle now emerges as a new organ that releases anti-inflammatory cytokines, such as IL-6 (interleukin-6). IL-6 inhibits TNF-α (tumour necrosis factor-α) production in adipose tissue and macrophages. The down-regulation of TNF-α induced by skeletal-muscle-derived IL-6 may also participate in mediating the atheroprotective effect of physical activity. © The Authors Journal compilation. © 2011 Biochemical Society.
Fanciullino A.L.,French National Institute for Agricultural Research |
Bidel L.P.R.,French National Institute for Agricultural Research |
Urban L.,University of Avignon
Plant, Cell and Environment | Year: 2014
Carotenoids play an important role in plant adaptation to fluctuating environments as well as in the human diet by contributing to the prevention of chronic diseases. Insights have been gained recently into the way individual factors, genetic, environmental or developmental, control the carotenoid biosynthetic pathway at the molecular level. The identification of the rate-limiting steps of carotenogenesis has paved the way for programmes of breeding, and metabolic engineering, aimed at increasing the concentration of carotenoids in different crop species. However, the complexity that arises from the interactions between the different factors as well as from the coordination between organs remains poorly understood. This review focuses on recent advances in carotenoid responses to environmental stimuli and discusses how the interactions between the modulation factors and between organs affect carotenoid build-up. We develop the idea that reactive oxygen species/redox status and sugars/carbon status can be considered as integrated factors that account for most effects of the major environmental factors influencing carotenoid biosynthesis. The discussion highlights the concept of carotenoids or carotenoid-derivatives as stress signals that may be involved in feedback controls. We propose a conceptual model of the effects of environmental and developmental factors on carotenoid build-up in fruits. This review presents an assessment of the current understanding of how the different environmental factors and their interactions influence carotenoid accumulation at the organ level. We develop the idea that environmental factors converge to modulate reactive oxygen species (ROS)/redox status (influenced by oxidative stress), and sugars/carbon status (which results from the balance between carbon gains and losses, and allocation between competing organs) and in this way regulate carotenoid accumulation. The discussion highlights the concept of carotenoids or carotenoid-derivatives as stress signals that may be involved in feedback controls. We propose a conceptual model of the effects of environmental and developmental factors that accounts for the known roles played by ROS and sugars on carotenoid build-up in fruits. © 2013 John Wiley & Sons Ltd.
Benslimane A.,University of Avignon |
Taleb T.,NEC Europe Ltd. |
Sivaraj R.,Tata Consultancy Services Ltd.
IEEE Journal on Selected Areas in Communications | Year: 2011
Coupling the high data rates of IEEE 802.11p-based VANETs and the wide coverage area of 3GPP networks (e.g., UMTS), this paper envisions a VANET-UMTS integrated network architecture. In this architecture, vehicles are dynamically clustered according to different related metrics. From these clusters, a minimum number of vehicles, equipped with IEEE 802.11p and UTRAN interfaces, are selected as vehicular gateways to link VANET to UMTS. Issues pertaining to gateway selection, gateway advertisement and discovery, service migration between gateways (i.e., when serving gateways lose their optimality) are all addressed and an adaptive mobile gateway management mechanism is proposed. Simulations are carried out using NS2 to evaluate the performance of the envisioned architecture incorporating the proposed mechanisms. Encouraging results are obtained in terms of high data packet delivery ratios and throughput, reduced control packet overhead, and minimized delay and packet drop rates. © 2011 IEEE.
Arnaud M.-C.,University of Avignon
Nonlinearity | Year: 2011
Let H : T * M → ℝ be a Tonelli Hamiltonian defined on the cotangent bundle of a compact and connected manifold and let u : M → ℝ be a semi-concave function. If ε(u) is the set of all the super-differentials of u and (φ t ) the Hamiltonian flow of H, we prove that for t > 0 small enough, φ -t (ε(u)) is an exact Lagrangian Lipschitz graph. This provides a geometric interpretation/ explanation of a regularization tool that was introduced by Bernard (2007 Ann. Sci. Ećole Norm. Sup. 40445-52) to prove the existence of C 1,1 subsolutions. © 2011 IOP Publishing Ltd & London Mathematical Society.