HIL Validation of embedded software. Application on hybrid industrial vehicle.

site de la Conférence : http://ettap09.inrets.frInternational audienceCurrent requirements of ecology and mobility are at the basis of the development of less polluting vehicles. In most of the cases, these vehicles need a clever and optimized energy management, which can be reached thanks to a more complex electronic embedded system. That is why, a special care on electronics reliability is required to ensure a good product quality. In this paper, we will focus on a systematic reasoning to obtain a suited test bench for covering the verification of a complete set of embedded electronics functional specification of a hybrid powertrain. The HIL (Hardware In the Loop) test bench enables the control unit environment in real time to be simulated and their closed loop behavior in wished situations to be studied. Based on control unit and system specifications, the method describes how to define the HIL platform in terms of hardware interface and internal behavior (models)

Endothelial plasticity drives arterial remodeling within the endocardium after myocardial infarction.

International audienceRATIONALE:Revascularization of injured, ischemic, and regenerating organs is essential to restore organ function. In the postinfarct heart, however, the mechanisms underlying the formation of new coronary arteries are poorly understood.OBJECTIVE:To study vascular remodeling of coronary arteries after infarction.METHODS AND RESULTS:We performed permanent left coronary ligation on Connexin40-GFP mice expressing green fluorescent protein (GFP) in endothelial cells of coronary arteries but not veins, capillaries, or endocardium. GFP(+) endothelial foci were identified within the endocardium in the infarct zone. These previously undescribed structures, termed endocardial flowers, have a distinct endothelial phenotype (Cx40(+), VEGFR2(+), and endoglin(-)) to the surrounding endocardium (Cx40(-), VEGFR2(-), and endoglin(+)). Endocardial flowers are contiguous with coronary vessels and associated with subendocardial smooth muscle cell accumulation. Genetic lineage tracing reveals extensive endothelial plasticity in the postinfarct heart, showing that endocardial flowers develop by arteriogenesis of Cx40(-) cells and by outgrowth of pre-existing coronary arteries. Finally, endocardial flowers exhibit angiogenic features, including early VEGFR2 expression and active proliferation of adjacent endocardial and smooth muscle cells.CONCLUSIONS:Arterial endothelial foci within the endocardium reveal extensive endothelial cell plasticity in the infarct zone and identify the endocardium as a site of endogenous arteriogenesis and source of endothelial cells to promote vascularization in regenerative strategies

Machine Drive System Modelling for HIL Simulation

International audienceThis paper presents bond-graph models of a parallel hybrid powertrain developed by Volvo Powertrain. It will first focus on bond-graph model of an electrical machine and its characteristic equations. Then a converter representation will be added to the bond-graph to get a complete machine drive system bond-graph model adapted to a HIL application. The closed loop will also be presented and the process of validation based on supplier data will be explained. Finally, we will conclude with an overview of the complete driveline model based on bond graph

Mineralocorticoid receptor antagonism prevents the electrical remodeling that precedes cellular hypertrophy after myocardial infarction.

International audienceBackground— Cardiac hypertrophy underlies arrhythmias and sudden death, for which mineralocorticoid receptor (MR) activity has recently been implicated. We sought to establish the sequence of ionic events that link the initiating insult and MR to hypertrophy development. Methods and Results— Using whole-cell, patch-clamp and quantitative reverse transcription–polymerase chain reaction techniques on right ventricular myocytes of a myocardial infarction (MI) rat model, we examined the cellular response over time. One week after MI, no sign of cellular hypertrophy was found, but action potential duration (APD) was lengthened. Both an increase in Ca 2+ current ( I Ca ) and a decrease in K + transient outward current ( I to ) underlay this effect. Consistently, the relative expression of mRNA coding for the Ca 2+ channel α1C subunit (Ca v 1.2) increased, and that of the K + channel K v 4.2 subunit decreased. Three weeks after MI, AP prolongation endured, whereas cellular hypertrophy developed. I Ca density, Ca v 1.2, and K v 4.2 mRNA levels regained control levels, but I to density remained reduced. Long-term treatment with RU28318, an MR antagonist, prevented this electrical remodeling. In a different etiologic model of abdominal aortic constriction, we confirmed that APD prolongation and modifications of ionic currents precede cellular hypertrophy. Conclusions— Electrical remodeling, which is triggered at least in part by MR activation, is an initial, early cellular response to hypertrophic insults

Early signs of cardiac diastolic dysfunction in ovariectomized WKY and SHR female rats.

Half of patients with heart failure (HF) have diastolic dysfunction but preserved EF (> 50%; HFpEF). There is no specific treatment. Aging populations, and particularly women, are more widely concerned. Why are women more likely than men to develop HFpEF? Despite possible limitations, small animal models could provide comprehensive approaches to identify/test novel therapeutic targets

Cardioprotection following injury heart failure afforded by a non-enzymatic oxygenated metabolite of omega 3 fatty acid involves ryanodine receptor mechanism and Mitochondrial Function

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