Pollution and pollutant transport in the geosphere - An introduction to the symposium

Environmental research in earth sciences is focused on the geosphere, i.e. (1) waters and sediments of rivers, lakes and oceans, and (2) soils and underlying shallow rock formations,both water-unsaturated and -saturated. The subsurface is studied down to greater depths at sites where waste repositories or tunnels are planned and mining activities exist. In recent years, earth scientists have become more and more involved in pollution problems related to their classical field of interest, e.g. groundwater, ore deposits, or petroleum and non-metal natural deposits (gravel, clay, cement precursors). Major pollutants include chemical substances, radioactive isotopes and microorganisms. Mechanisms which govern the transport of pollutants are of physical, chemical (dissolution, precipitation, adsorption), or microbiological (transformation) nature. Land-use planning must reflect a sustainable development and sound scientific criteria. Today's environmental pollution requires working teams with an interdisciplinary background in earth sciences, hydrology, chemistry, biology, physics as well as engineering. This symposium brought together for the first time in Switzerland earth and soil scientists, physicists and chemists, to present and discuss environmental issues concerning the geosphere.

Brain Glucose Transport and Phosphorylation Under Acute Insulin-Induced Hypoglycemia in Mice: An 18F-FDG PET Study.

We addressed the questions of how cerebral glucose transport and phosphorylation change under acute hypoglycemia and what the underlying mechanisms of adaptation are. METHODS: Quantitative (18)F-FDG PET combined with the acquisition of real-time arterial input function was performed on mice. Hypoglycemia was induced and maintained by insulin infusion. PET data were analyzed with the 2-tissue-compartment model for (18)F-FDG, and the results were evaluated with Michaelis-Menten saturation kinetics. RESULTS: Glucose clearance from plasma to brain (K1,glc) and the phosphorylation rate constant increased with decreasing plasma glucose (Gp), in particular at a Gp of less than 2.5 mmol/L. Estimated cerebral glucose extraction ratios taking into account an increased cerebral blood flow (CBF) at a Gp of less than 2 mmol/L were between 0.14 and 0.79. CBF-normalized K1,glc values were in agreement with saturation kinetics. Phosphorylation rate constants indicated intracellular glucose depletion at a Gp of less than 2-3 mmol/L. When brain regions were compared, glucose transport under hypoglycemia was lowest in the hypothalamus. CONCLUSION: Alterations in glucose transport and phosphorylation, as well as intracellular glucose depletion, under acute hypoglycemia can be modeled by saturation kinetics taking into account an increase in CBF. Distinct transport kinetics in the hypothalamus may be involved in its glucose-sensing function.

Rebound and disinvestment effects in oil consumption and supply resulting from an increase in energy efficiency in the Scottish commercial transport sector

In this paper we use an energy-economy-environment computable general equilibrium (CGE) model of the Scottish economy to examine the impacts of an exogenous increase in energy augmenting technological progress in the domestic commercial Transport sector on the supply and use of energy. We focus our analysis on oil, as the main type of energy input used in commercial transport activity. We find that a 5% increase in energy efficiency in the commercial Transport sector leads to rebound effects in the use of oil-based energy commodities in all time periods, in the target sector and at the economy-wide level. However, our results also suggest that such an efficiency improvement may cause a contraction in capacity in the Scottish oil supply sector. This ‘disinvestment effect’ acts as a constraint on the size of rebound effects. However, the magnitude of rebound effects and presence of the disinvestment effect in the simulations conducted here are sensitive to the specification of key elasticities of substitution in the nested production function for the target sector, particularly the substitutability of energy for non-energy intermediate inputs to production.

PKS2: A link between phototropin signalling and auxin transport - a study on how plants sense and respond to light.

The blue light photoreceptors phototropins (phot1 and phot2 in Arabidopsis thaliana (L.)) carry out various light responses of great adaptive value that optimize plant growth. These processes include phototropism (the bending of an organ induced by unequal light distribution), chloroplast movements, stomatal opening, leaf flattening and solar tracking. The biochemical pathways controlling these important blue light responses are just starting to be elucidated. The PHYTOCHROME KINASE SUBSTRATE (PKS1-4) proteins - the subject of this research - have recently been identified as novel phototropism signalling components. PKS1 (the founding member of this family) interacts in a same complex in vivo with phot1 and the important phot1 signalling element NON-PHOTOTROPIC HYPOCOTYL 3 (NPH3). This suggested that the PKS may act as early components of phot signalling. This work further investigates the role of this protein family during phototropin signalling Genetic experiments clearly showed that the PKS do not control chloroplast movements or stomatal opening. However, PKS2 plays a critical role with NPH3 during leaf flattening and solar tracking. Epistasis data indicated that both proteins act in phot1 and phot2 pathways, which is consistent with their in vivo interaction with both phototropins. Because phototropism, leaf flattening and solar tracking are developmental processes regulated by the hormone auxin, the role of PKS2 and NPH3 during auxin homeostasis was also investigated. Interestingly, PKS2 loss-of-function restores leaf flattening in the auxin transporter mutant aux1. Moreover, PKS2 and NPH3 are found in a same complex with AUX1 in vivo. Taken together, these results suggest that PKS2 may act with NPH3 as a connecting point between phot signalling and auxin transport. Further experiments were performed to explore the molecular mode of action of PKS2 and NPH3 in this process. The significance of these results is discussed.

Sarcopromusca pruna (Diptera: Muscidae) as an egg transport host of Dermatobia hominis (Diptera: Cuterebridae) in the cacau region of Bahia, Brazil

Sarcopromusca pruna appears to be the predominant transport host for Dermatobia hominis eggs among cattle herds in central eastern Bahia, Brazil. In the study area, two seasonal peaks of S. Pruna abundance coincide with those of Dermatobia, from mid July through late September and from mid November until early January, two periods of moderate monthly rainfall between anual extremes. Among more than 26,000 flies examined during the study, 75 (all female S. pruna) bore Dermatobia eggs. Certain aspects of Dermatobia behavior and ovoposition habits in the field are also discussed.

Protease-activated receptor 2 signalling promotes dendritic cell antigen transport and T cell activation in vivo

Rapport de synthèse : Le récepteur activé par protéase de type 2 (PAR2) intervient dans l'inflammation dans divers modèles expérimentaux de maladies inflammatoires et auto-immunes, mais le mécanisme par lequel il exerce cette fonction reste mal compris. PAR2 est exprimé sur des cellules endothéliales et immunitaires et a été impliqué dans la différentiation des cellules dendritiques (DC). Avec leur rôle central dans la réponse immune, les DC pourraient jouer un rôle clef, l'activation de PAR2 à leur surface modulant la réponse immune. Des recherches précédentes ont montré que PAR2 a un effet dans le développement et la maturation des DC de moelle osseuse in vitro, ainsi que dans la promotion de la réponse immune en allergie. Dans cette étude, nous avons évalué l'impact in vivo de l'activation de PAR2 sur les DC et les cellules T dans des souris déficientes en PAR2 (KO) en utilisant un peptide agoniste spécifique du PAR2 (AP2). L'activation de PAR2 a augmenté la fréquence de DC matures dans les ganglions lymphatiques 24 heures après l'administration d'AP2 d'une manière significative. En outre, ces DC avaient une expression augmentée des molécules de co-stimulation CD86 et du complexe majeur d'histocompatibilité type 2 (MHC-II). 48 heures après l'injection d'AP2, nous avons également observé une élévation significative des lymphocytes T CD4+ et CD8+ activés, (CD44+CD62-) dans ces ganglions. Des changements dans le profil d'activation des DC et des cellules T n'ont pas été observés au niveau de a rate. L'influence de la signalisation de PAR2 sur le transport d'antigène aux ganglions lymphatiques inguinaux a été évaluée dans le contexte d'hypersensibilité retardée de type IV. Les souris KO sensibilisées par peinture de la peau avec fluorescéine isothyocyanate (FITC) afin d'induire une hypersensibilité retardée avaient un pourcentage diminué de DC FITC+ dans les ganglions lymphatiques 24 heures après l'application du FITC en comparaison avec les souris sauvages avec le même fond génétique (0.47% vs 0.95% des cellules ganglionnaires totales). En conclusion, ces résultats démontrent que la signalisation de PAR2 favorise et renforce la maturation et le transport d'antigène par des DC .vers les ganglions lymphatiques ainsi que l'activation ultérieure des lymphocytes T, et de ce fait fournissent une explication pour l'effet pro inflammatoire de PAR2 dans les modèles animaux d'inflammation. Une meilleure compréhension de ce mécanisme de modulation du système immun via PAR2 peut s'avérer particulièrement utile pour le développement des vaccins, ainsi que pour la découverte de nouvelles cibles thérapeutiques dans le contexte de l'allergie, l'auto-immunité, et les maladies inflammatoires.

Quantifying rates of landscape evolution and tectonic processes by thermochronology and numerical modeling of crustal heat transport using PECUBE

PECUBE is a three-dimensional thermal-kinematic code capable of solving the heat production-diffusion-advection equation under a temporally varying surface boundary condition. It was initially developed to assess the effects of time-varying surface topography (relief) on low-temperature thermochronological datasets. Thermochronometric ages are predicted by tracking the time-temperature histories of rock-particles ending up at the surface and by combining these with various age-prediction models. In the decade since its inception, the PECUBE code has been under continuous development as its use became wider and addressed different tectonic-geomorphic problems. This paper describes several major recent improvements in the code, including its integration with an inverse-modeling package based on the Neighborhood Algorithm, the incorporation of fault-controlled kinematics, several different ways to address topographic and drainage change through time, the ability to predict subsurface (tunnel or borehole) data, prediction of detrital thermochronology data and a method to compare these with observations, and the coupling with landscape-evolution (or surface-process) models. Each new development is described together with one or several applications, so that the reader and potential user can clearly assess and make use of the capabilities of PECUBE. We end with describing some developments that are currently underway or should take place in the foreseeable future. (C) 2012 Elsevier B.V. All rights reserved.

Normal kinetics of intestinal glucose absorption in the absence of GLUT2: evidence for a transport pathway requiring glucose phosphorylation and transfer into the endoplasmic reticulum.

Glucose is absorbed through the intestine by a transepithelial transport system initiated at the apical membrane by the cotransporter SGLT-1; intracellular glucose is then assumed to diffuse across the basolateral membrane through GLUT2. Here, we evaluated the impact of GLUT2 gene inactivation on this transepithelial transport process. We report that the kinetics of transepithelial glucose transport, as assessed in oral glucose tolerance tests, was identical in the presence or absence of GLUT2; that the transport was transcellular because it could be inhibited by the SGLT-1 inhibitor phlorizin, and that it could not be explained by overexpression of another known glucose transporter. By using an isolated intestine perfusion system, we demonstrated that the rate of transepithelial transport was similar in control and GLUT2(-/-) intestine and that it was increased to the same extent by cAMP in both situations. However, in the absence, but not in the presence, of GLUT2, the transport was inhibited dose-dependently by the glucose-6-phosphate translocase inhibitor S4048. Furthermore, whereas transport of [(14)C]glucose proceeded with the same kinetics in control and GLUT2(-/-) intestine, [(14)C]3-O-methylglucose was transported in intestine of control but not of mutant mice. Together our data demonstrate the existence of a transepithelial glucose transport system in GLUT2(-/-) intestine that requires glucose phosphorylation and transfer of glucose-6-phosphate into the endoplasmic reticulum. Glucose may then be released out of the cells by a membrane traffic-based pathway similar to the one we previously described in GLUT2-null hepatocytes.

The Accessibility City. When Transport Infrastructure Matters in Urban Spatial Structure

Suburbanization is changing the urban spatial structure and less monocentric metropolitan regions are becoming the new urban reality. Focused only on centers, most works have studied these spatial changes neglecting the role of transport infrastructure and its related location model, the “accessibility city”, in which employment and population concentrate in low-density settlements and close to transport infrastructure. For the case of Barcelona, we consider this location model and study the population spatial structure between 1991 and 2006. The results reveal a mix between polycentricity and the accessibility city, with movements away from the main centers, but close to the transport infrastructure.

Iceberg transport technologies in spatial competition. Hotelling reborn

Transport costs in address models of differentiation are usually modeled as separable of the consumption commodity and with a parametric price. However, there are many sectors in an economy where such modeling is not satisfactory either because transportation is supplied under oligopolistic conditions or because there is a difference (loss) between the amount delivered at the point of production and the amount received at the point of consumption. This paper is a first attempt to tackle these issues proposing to study competition in spatial models using an iceberg-like transport cost technology allowing for concave and convex melting functions.

Transport pathways in the malaria-infected erythrocyte: characterization and their use as potential targets for chemotherapy

The intraerythrocytic malarial parasite is involved in an extremely intensive anabolic activity while it resides in its metabolically quiescent host cell. The necessary fast uptake of nutrients and the discharge of waste product, are guaranteed by parasite-induced alterations of the constitutive transporters of the host cell and the production of new parallel pathways. The membrane of the host cell thus becomes permeable to phospholipids, purine bases and nucleosides, small non-electrolytes, anions and cations. When the new pathways are quantitatively unimportant, classical inhibitors of native transporters can be used to inhibit parasite growth. Several compounds were found to effectively inhibit the new pathways and consequently, parasite growth. The pathways have also been used to introduce cytotoxic agents. The parasitophorous membrane consists of channels which are highly permeable to small solutes and display no ion selectivity. Transport of some cations and anions across the parasite membrane is rapid and insensitive to classical inhibitors, and in some cases it is mediated by specific antiporters which respond to their respective inhibitors. Macromolecules have been shown to reach the parasitophorous space through a duct contiguous with the host cell membrane, and subsequently to be endocytosed at the parasite membrane. The simultaneous presence of the parasitophorous membrane channels and the duct, however, is incompatible with experimental evidences. No specific inhibitors were found as yet that would efficiently inhibit transport through the channels or the duct.

Glutamate Transport Decreases Mitochondrial pH and Modulates Oxidative Metabolism in Astrocytes.

During synaptic activity, the clearance of neuronally released glutamate leads to an intracellular sodium concentration increase in astrocytes that is associated with significant metabolic cost. The proximity of mitochondria at glutamate uptake sites in astrocytes raises the question of the ability of mitochondria to respond to these energy demands. We used dynamic fluorescence imaging to investigate the impact of glutamatergic transmission on mitochondria in intact astrocytes. Neuronal release of glutamate induced an intracellular acidification in astrocytes, via glutamate transporters, that spread over the mitochondrial matrix. The glutamate-induced mitochondrial matrix acidification exceeded cytosolic acidification and abrogated cytosol-to-mitochondrial matrix pH gradient. By decoupling glutamate uptake from cellular acidification, we found that glutamate induced a pH-mediated decrease in mitochondrial metabolism that surpasses the Ca(2+)-mediated stimulatory effects. These findings suggest a model in which excitatory neurotransmission dynamically regulates astrocyte energy metabolism by limiting the contribution of mitochondria to the metabolic response, thereby increasing the local oxygen availability and preventing excessive mitochondrial reactive oxygen species production.