Search

For residential customers living in a cold climate, energy savings during the heating season are often achieved through thermostat setbacks. In order to gain insight into this phenomenon, the Laboratoire des Technologies de l’Energie (LTE) of Hydro-Quebec has used its unique twin-houses test bench that consists of two all-electric single-family houses heated by baseboards individually controlled in each room by a line-voltage electronic thermostat. The objective of this paper is to evaluate and analyse three different thermostat setback scenarios of 4 °C (night, day and dual setbacks) using in-situ measurements at the LTE twin-houses facility. The results show that at the house level, savings of 10 ± 5.9% were possible for day time and night time setbacks, while being more important for dual setback scenarios. The obtained results also show that the savings and comfort conditions varied greatly from one floor to another.

Blockade of interleukin (IL)-23 or IL-17 with biologics is clinically validated as a treatment of psoriasis. However, the clinical impact of targeting other nodes within the IL-23/IL-17 pathway, especially with small molecules, is less defined. We report on a novel small molecule inverse agonist of retinoid acid–related orphan receptor (ROR) γt and its efficacy in preclinical models of psoriasis and arthritis. 1-(2,4-Dichloro-3-((1,4-dimethyl-6-(trifluoromethyl)-1H-indol-2-yl)methyl)benzoyl)piperidine-4-carboxylic acid (A-9758) was optimized from material identified from a high-throughput screening campaign. A-9758 is selective for RORγt and exhibits robust potency against IL-17A release both in vitro and in vivo. In vivo, we also show that IL-23 is sufficient to drive the accumulation of RORγt+ cells, and inhibition of RORγt significantly attenuates IL-23–driven psoriasiform dermatitis. Therapeutic treatment with A-9758 (i.e., delivered during active disease) was also effective in blocking skin and joint inflammation. Finally, A-9758 exhibited efficacy in an ex vivo human whole blood assay, suggesting small molecule inverse agonists of RORγt could be efficacious in human IL-17–related diseases. SIGNIFICANCE STATEMENT Using a novel small molecule inverse agonist, and preclinical assays, we show that RORγt is a viable target for the inhibition of RORγt/Th17–driven diseases such as psoriasis. Preclinical models of psoriasis show that inhibition of RORγt blocks both the accumulation and effector function of IL-17–producing T cells.

Estimating the impact of pest insects on forest productivity requires a better understanding of host tree responses. While many studies have focused on juvenile trees, studying the impacts of defoliation on trees of increasing age helps to better characterize underlying mechanisms regulating growth responses to defoliation. During winter 2009–2010 a large outbreak of pine processionary moth occurred in Southwestern France. We established a field experiment to examine the effects of pine processionary moth defoliation varying from 25% to 100% on the growth of Pinus pinaster in stands ranging from 3 to 40 years old. Our results showed that pine processionary moth defoliation resulted in significant loss of radial growth for at least two years following defoliation. Stem growth loss in the first and second years was proportional to defoliation intensity and ranged from 32% to 93% in year 1, and from 17% to 68% in year 2. Stem growth was most reduced in older trees. Carbohydrates and nitrogen contents in needles and stem sapwood were also affected by defoliation. Our results suggest that defoliation affects stem growth through nitrogen and carbon resource limitation and that stem growth would be a lower priority sink for resources than other physiological processes in pine trees.

This paper presents a fault-tolerant control system built using a novel redundancy scheme and draws a comparison with a traditional solution by means of both qualitative and quantitative analysis. Either system comprises three interconnected electronic control units (ECUs) and two redundant actuators. The position of the attached mechanics is measured by redundant position sensors, thus closing the control loop. In case of an error (detected through observing rotational sensors), actuators may be passivated by retracting the power supply via associated output stages.While the traditional system under investigation is built rather conservatively, with a high degree of redundancy (overall, 14 components are used), the novel approach requires only 11 components and no crosswise wiring at all. In the novel design, encrypted communication channels convert all byzantine faults into crash faults. It will be shown that such a system is without a single point of failure, i.e. at least two components must f...

International audience; The pine processionary moth is, by far, the most important insect defoliator of pine forests in Southern Europe and North Africa, both in terms of its temporal occurrence, geographic range and socioeconomic impact. Monitoring and pest management actions are therefore required on a regular basis, to ensure the detection, evaluation and mitigation of potential risks to forest and public health. However, we still lack some of the basic knowledge required for relevant analyses of the risk posed by the pine processionary moth. Pest risk is defined as a combination of three components: (1) pest occurrence, which depends on the spatiotemporal dynamics of populations; (2) plant vulnerability to the pest, resulting in a certain amount of damage; and (3) the socioeconomic impact of damage, depending on the potential value of the plants damaged (Jactel et al. 2012). The population dynamics of the processionary moth has been extensively studied, in particular within the context of climate change (see Battisti et al. 2014, Chap. 2, this volume). Several studies have recently addressed the question of tree and forest vulnerability to pine processionary attacks but a comprehensive review of evidence was missing. This is the first objective of this chapter. In particular we were interested in a better understanding of the ecological mechanisms responsible for the host tree selection, at both the species and individual tree levels. In a second part we show that pine susceptibility to the pine processionary moth could be reduced by improving forest diversity at different spatial scales. In the last part of this chapter we provide quantitative estimate of the growth losses caused by defoliations of the pine processionary moth. Altogether this information paves the way for quantitative risk analyses on pine processionary moth infestations based on forest growth models.

International audience; Climate change is expected to increase both pest insect damage and the occurrence of severe drought. There is therefore a need to better understand the combined effects of biotic and abiotic damage on tree growth in order to predict the multi--factorial effect of climate change on forest ecosystem productivity. Indeed, the effect of stress interactions on tree growth is an increasingly important topic that greatly lacks experiments and data, and it is unlikely that the impact of combined stresses can be extrapolated from the outcomes of studies that focused on a single stress. We developed an original manipulative study under real field conditions where we applied artificial defoliation and induced water stress on 10-year-old (similar to 10 m high) maritime pine trees (Pinus pinaster Ait.). Tree response to combined stresses was quantitatively assessed following tree secondary growth and carbohydrate pools. Such a design allowed us to address the crucial question of combined stresses on trees under stand conditions, sharing soil supplies with neighboring trees. Our initial hypotheses were that (i) moderate defoliation can limit the impact of water stress on tree growth through reduced transpiration demand by a tree canopy partly defoliated and that (ii) defoliation results in reduced non-structural carbohydrate (NSC) pools, affecting tree tolerance to drought. Our results showed additive effects of defoliation and water stress on tree growth and contradict our initial hypothesis. Indeed, under stand conditions, we found that partial defoliation does not limit the impact of water stress through reduced transpiration. Our study also highlighted that, even if NSC in all organs were affected by defoliation, tree response to water stress was not triggered. We found that stem NSC were maintained or increased during the entire growing season, supporting literature-based hypotheses such as an active maintenance of the hydraulic system or another limiting resource for tree growth under defoliation. We also observed a significant decrease in root carbohydrates, which suggests a shift in the root carbon balance under defoliation. The decrease in carbohydrate supply under defoliation may not counterbalance the carbon use for mineral and water uptakes or a translocation to other tissues.

National audience

International audience; • Context Forests are important carbon sinks, but increasing temperatures may favour increases in insect populations, resulting in greater damage to trees. This, in turn, would lead to lower levels of carbon sequestration, intensifying global warming. • Aim It is therefore important to predict the impact of insect defoliation on tree growth accurately. The main insect defoliators of conifers in Southern Europe and North Africa are pine and cedar processionary moths (Lepidoptera, Thaumetopoeidae). • Method We conducted a meta-analysis based on 45 study cases, to estimate the effect of processionary moth defoliation on tree growth. • Result Overall, processionary moth defoliation had a significant impact on tree growth, regardless of the tree and moth species considered. Mean relative tree growth loss increased with the rate of defoliation levelling out at ca. 50 %; it was significantly larger for young than for old trees. • Conclusion These results suggest that estimates of processionary moth defoliation could easily be incorporated into tree growth models, to predict the effect of processionary moth outbreaks on carbon sequestration in Mediterranean forests.

We present a dual-band (Cellular & PCS) dual-path zero-IF receiver for CDMA2000 diversity, monitoring and simultaneous-GPS. The secondary path is a SAW-less diversity CDMA receiver which can be also used for advanced features like monitoring when supported with an additional external VCO. A GPS receiver is integrated with its dedicated VCO allowing simultaneous positioning during a cellular call. The circuit is implemented in a 0.25μm 40GHz-fT BiCMOS process and uses a HVQFN 56-pin package. It consumes a maximum 300mW from a 2.8V supply in dual-modes. The chip area is 12.8mm2., {"references":["CDMA2000 Standard 3GPP2 C.S0033.","W. Y. Ali-Ahmad, \"The CDMA receiver system in a IS-98-A standard,\"\nElectronics Engineer, July 2000.","H. Waite et al., \"A CDMA2000 zero-IF receiver with low-leakage\nintegrated front-end,\" IEEE JSSC, pp. 1175-1179, July 2004.","O. Charlon et al, \"A dual-mode zero-IF receiver for dual-band CDMA\ncellular and GPS,\" IEEE ESSCIRC, pp. 432-435, Sept. 2007.","Y. Xu et al., \"A low-IF CMOS simultaneous GPS receiver integrated in\na multimode transceiver,\" IEEE CICC, pp. 107-110, 2007."]}

Sub-Riemannian distances are obtained by minimizing length of curves whose velocity is constrained to be tangent to a given sub-bundle of the tangent bundle. We study the regularity properties of the function x ↦ d(x 0, x) for a given sub-Riemannian distance d on a neighborhood of a point x 0 of a manifold M. We already know that this function is not C 1 on any neighborhood of x 0 (see [1]) and even if the data are analytic, the distance may fail to be subanalytic [8]. In this paper we make the link between the singular support of x ↦ d(x 0, x), the cut locus and the set of points reached from x 0 by singular minimizers.

Cell surface receptors for high-density lipoprotein (HDL) on hepatocytes are major partners in the regulation of cholesterol homeostasis. We recently identified a cell surface ATP synthase as a high-affinity receptor for HDL apolipoprotein A-I (apoA-I) on human hepatocytes. Stimulation of this ectopic ATP synthase by apoA-I triggered a low-affinity-receptor-dependent HDL endocytosis by a mechanism strictly related to the generation of ADP. This suggests that nucleotide G-protein-coupled receptors of the P2Y family are molecular components in this pathway. Only P2Y1 and P2Y13 are present on the membrane of hepatocytes. Using both a pharmacological approach and small interference RNA, we identified P2Y13 as the main partner in hepatic HDL endocytosis, in cultured cells as well as in situ in perfused mouse livers. We also found a new important action of the antithrombotic agent AR-C69931MX as a strong activator of P2Y13-mediated HDL endocytosis.

Fas (CD95)-induced hepatocyte apoptosis and cytotoxic activity of neutrophils infiltrating the injured liver are two major events leading to hepatitis. Because it has been reported that opioids, via a direct interaction, sensitize splenocytes to Fas-mediated apoptosis by upregulating Fas messenger RNA (mRNA) and modulated neutrophil activity, we assumed that opioids may participate in the pathophysiology of hepatitis. Using the hepatitis model induced by agonistic anti-Fas antibody in mice, we showed that opioid receptor blockade reduced liver damage and consequently increased the survival rate of animals when the antagonist naltrexone was injected simultaneously or prior to antibody administration. Treatment of mice with morphine enhanced mortality. Naloxone methiodide-a selective peripheral opioid antagonist-had a protective effect, but the absence of opioid receptors in the liver, together with lack of morphine effect in Fas-induced apoptosis of primary cultured hepatocytes, ruled out a direct effect of opioids on hepatocytes. In addition, the neutralization of opioid activity by naltrexone did not modify Fas mRNA expression in the liver as assessed with real-time quantitative polymerase chain reaction. Injured livers were infiltrated by neutrophils, but granulocyte-depleted mice were not protected against the enhancing apoptotic effect of morphine. In conclusion, opioid receptor blockade improves the resistance of mice to Fas-induced hepatitis via a peripheral mechanism that does not involve a down-modulation of Fas mRNA in hepatocytes nor a decrease in proinflammatory activity of neutrophils.

High-density lipoprotein (HDL) cholesterol is an independent negative risk factor for coronary artery disease and thus represents today the only protective factor against atherosclerosis. The protective effect of HDL is mostly attributed to its central function in reverse cholesterol transport (RCT), a process whereby excess cell cholesterol is taken up and processed in HDL particles, and is later delivered to the liver for further metabolism and bile excretion. This process relies on specific interactions between HDL particles and cells, both peripheral (cholesterol efflux) and hepatic (cholesterol disposal) cells, and on the maturation of HDL particles within the vascular compartment. The plasma level of HDL cholesterol will thus result also from the complex interplay with cellular partners. Among them, some contribute to HDL formation - for instance ATP binding cassette AI protein - while others are mostly involved in HDL catabolism, the scavenger receptor-class B type I or the recently described membrane-bound ATP synthase/hydrolase. The last decade has seen major breakthroughs in the identification and elucidation of the role of cellular partners of HDL metabolism, and in their transcriptional regulations, opening up new perspectives in the modulation of HDL cholesterol.

International audience; The effect of high-density lipoprotein (HDL) in protecting against atherosclerosis is usually attributed to its role in ‘reverse cholesterol transport’1. In this process, HDL particles mediate the efflux and the transport of cholesterol from peripheral cells to the liver for further metabolism and bile excretion. Thus, cellsurface receptors for HDL on hepatocytes are chief partners in the regulation of cholesterol homeostasis2. A high-affinity HDL receptor for apolipoprotein A-I (apoA-I) was previously identified on the surface of hepatocytes3,4. Here we show that this receptor is identical to the b-chain of ATP synthase, a principal protein complex of the mitochondrial inner membrane. Different experimental approaches confirm this ectopic localization of components of the ATP synthase complex and the presence of ATP hydrolase activity at the hepatocyte cell surface. Receptor stimulation by apoA-I triggers the endocytosis of holo-HDL particles (protein plus lipid) by a mechanism that depends strictly on the generation of ADP. We confirm this effect on endocytosis in perfused rat liver ex vivo by using a specific inhibitor of ATP synthase. Thus, membrane-bound ATP synthase has a previously unsuspected role in modulating the concentrations of extracellular ADP and is regulated by a principal plasma apolipoprotein.

International audience