Editorial: Towards energy efficient and sustainable transportation networks

This special issue of the European Journal of Transport and Infrastructure Research comprises six papers, with a focus on energy efficiency and sustainability in transportation networks. Preliminary versions of those papers were presented during the EWGT 2012 Conference, the 15th meeting of the Euro Working Group on Transportation. The contributions have been selected to reflect the diversity of topics and approaches presented during the conference. They have been substantially extended by their respective authors and carefully reviewed and revised; this special issue contains the final selection of accepted papers. The editors are grateful to the authors and referees for their prompt and careful collaboration during the preparation of this special issue. This editorial first provides a few additional words about the Euro Working Group on Transportation and about the EWGT 2012 Conference, and then presents the selected contributions

Assessing the Impact of Speed Limit Changes on Urban Motorways: A Simulation Study in Lille, France

AbstractRecent directives in France on sustainable development have driven local Authorities to the reduction of speed limits on urban highways. Consequently, Local Authorities are interested in a thorough evaluation of this measure and in the estimation of the potential impact upon traffic and emissions.In this paper, we undertake an a priori evaluation of speed limit reduction from 110km/h to 90km/h on the Lille motorway network, in France. We first provide an overview of key lessons learned from previous speed limit reduction experiences. Then, we present the methodology of the specific prior evaluation on the Lille network. In particular, we use a first order macroscopic traffic simulation tool for this a priori assessment. The model is first calibrated and then statistically validated using traffic data. This statistical validation is consistent with good practices in simulation. The evaluation output allows for a thorough understanding of the impacts on prevailing traffic conditions and air pollution. Additional scenarios are also considered in order to take into account driver behaviour on the non-compliance with speed limits.Besides the various limitations of the study, especially those related to its predictive aspects, we can conclude that the intended measure will have a positive impact on traffic and emissions. Nevertheless, the magnitude of this impact is largely variable, in particular in regards to driver compliance

Does high-dose metformin cause lactic acidosis in type 2 diabetic patients after CABG surgery? A double blind randomized clinical trial

Metformin is a dimethyl biguanide oral anti-hyperglycemic agent. Lactic acidosis due to metformin is a fatal metabolic condition that limits its use in patients in poor clinical condition, consequently reducing the number of patients who benefit from this medication. In a double blind randomized clinical trial, we investigated 200 type 2 diabetic patients after coronary artery bypass surgery in the open heart ICU of the Mazandaran Heart Center, and randomly assigned them to equal intervention and control groups. The intervention group received regular insulin infusion along with 2 metformin 500 mg tablets every twelve hours, while the control group received only intravenous insulin with 2 placebo tablets every twelve hours. Lactate level, pH, base excess, blood glucose and serum creatinine were measured over five 12 h periods, with data averaged for each period. The primary outcome in this study was high lactate levels. Comparison between the 2 groups was made by independent Student’s t-test. To compare changes in multiple measures in each group and analysis of group interaction, a repeated measurement ANOVA test was used

Altered Mitochondrial Function, Mitochondrial DNA and Reduced Metabolic Flexibility in Patients With Diabetic Nephropathy.

The purpose of this study was to determine if mitochondrial dysfunction plays a role in diabetic nephropathy (DN), a kidney disease which affects > 100 million people worldwide and is a leading cause of renal failure despite therapy. A cross-sectional study comparing DN with diabetes patients without kidney disease (DC) and healthy controls (HCs); and renal mesangial cells (HMCs) grown in normal and high glucose, was carried out. Patients with diabetes (DC) had increased circulating mitochondrial DNA (MtDNA), and HMCs increased their MtDNA within 24 h of hyperglycaemia. The increased MtDNA content in DCs and HMCs was not functional as transcription was unaltered/down-regulated, and MtDNA damage was present. MtDNA was increased in DC compared to HC, conversely, patients with DN had lower MtDNA than DC. Hyperglycaemic HMCs had fragmented mitochondria and TLR9 pathway activation, and in diabetic patients, mitophagy was reduced. Despite MtDNA content and integrity changing within 4 days, hyperglycaemic HMCs had a normal bio-energetic profile until 8 days, after which mitochondrial metabolism was progressively impaired. Peripheral blood mononuclear cells (PBMCs) from DN patients had reduced reserve capacity and maximal respiration, loss of metabolic flexibility and reduced Bioenergetic Health Index (BHI) compared to DC. Our data show that MtDNA changes precede bioenergetic dysfunction and that patients with DN have impaired mitochondrial metabolism compared to DC, leading us to propose that systemic mitochondrial dysfunction initiated by glucose induced MtDNA damage may be involved in the development of DN. Longitudinal studies are needed to define a potential cause-effect relationship between changes in MtDNA and bioenergetics in DN

Preservation of microvascular barrier function requires CD31 receptor-induced metabolic reprogramming

Endothelial barrier (EB) breaching is a frequent event during inflammation, and it is followed by the rapid recovery of microvascular integrity. The molecular mechanisms of EB recovery are poorly understood. Triggering of MHC molecules by migrating T-cells is a minimal signal capable of inducing endothelial contraction and transient microvascular leakage. Using this model, we show that EB recovery requires a CD31 receptor-induced, robust glycolytic response sustaining junction re-annealing. Mechanistically, this response involves src-homology phosphatase activation leading to Akt-mediated nuclear exclusion of FoxO1 and concomitant \u3b2-catenin translocation to the nucleus, collectively leading to cMyc transcription. CD31 signals also sustain mitochondrial respiration, however this pathway does not contribute to junction remodeling. We further show that pathologic microvascular leakage in CD31-deficient mice can be corrected by enhancing the glycolytic flux via pharmacological Akt or AMPK activation, thus providing a molecular platform for the therapeutic control of EB response

Etude rétrospective des facteurs d'évolutivité à long terme et du traitement des GEM prises en charge entre 1981 et 2007 au CHRU de Lille

LILLE2-BU Santé-Recherche (593502101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF