Real-time monitoring data for real-time multi-model validation: coupling ENSEMBLE and EURDEP.

The ENSEMBLE system has been considerably expanded and improved. The system that allows the real-time collection of atmospheric dispersion forecasts their real-time consultation and ensemble dispersion analysis has been coupled with the EUropean Radiological Data Exchange Platform (EURDEP) for the acquisition of real-time monitoring data on environmental (mainly in air) radiological measurements. This paper explains how the coupling has been realized and presents the potentials of this unique system that is presently in use in more than 25 countries around the world.

An evaluation of particle deposition fluxes to cultural heritage sites in Florence, Italy.

The pernicious effects of deposition of airborne particles on monumental stones have been widely demonstrated, but estimates of deposition fluxes on historic buildings remain a hard task because of the lack of careful experiments and modelling. AERBOX is a new box model developed by ENVIROWARE and ENEA, simulating the whole life cycle of aerosols. AERBOX takes into account all the relevant chemical and physical processes involved: emission, chemical reactions in gas and in gas-liquid phases, deposition, entrainment, condensation and nucleation. Concentration and deposition rates of 52 species of gaseous pollutants and 14 species of particulate pollutants are calculated on hourly basis. A modelling system composed by AERBOX and the emission pre-processor Tool for Hourly Speciation of CORINAIR Annual Emissions (THOSCANE) has been applied to estimate the flux of particulate matter deposited on the monumental area of Florence downtown starting from a CORINAIR emission inventory developed by the Tuscany Region including the industrial and mobile sources in the area of Florence and Prato counties. The time and chemical profiles of the emissions have been adapted to the Tuscany region from the reference profiles given by both the California Air Resource Board and EPA and meteorological inputs were given by the Tuscany Meteorological Centre. Concentrations and deposition fluxes were compared with field measurements available in the open literature.

Can the confidence in long range atmospheric transport models be increased? The pan-european experience of ensemble.

Is atmospheric dispersion forecasting an important asset of the early-phase nuclear emergency response management? Is there a 'perfect atmospheric dispersion model'? Is there a way to make the results of dispersion models more reliable and trustworthy? While seeking to answer these questions the multi-model ensemble dispersion forecast system ENSEMBLE will be presented.

Forecasting the consequences of accidental releases of radionuclides in the atmosphere from ensemble dispersion modelling.

The RTMOD system is presented as a tool for the intercomparison of long-range dispersion models as well as a system for support of decision making. RTMOD is an internet-based procedure that collects the results of more than 20 models used around the world to predict the transport and deposition of radioactive releases in the atmosphere. It allows the real-time acquisition of model results and their intercomparison. Taking advantage of the availability of several model results, the system can also be used as a tool to support decision making in case of emergency. The new concept of ensemble dispersion modelling is introduced which is the basis for the decision-making application of RTMOD. New statistical parameters are presented that allow gathering the results of several models to produce a single dispersion forecast. The devised parameters are presented and tested on the results of RTMOD exercises.

Biochemical analysis of myelin lipids and proteins in a model of methyl donor pathway deficit: effect of S-adenosylmethionine.

S-Adenosylmethionine (SAMe) is the methyl donor to numerous acceptor molecules. We used cycloleucine (CL), which prevents the conversion of methionine to SAMe by inhibiting ATP-l-methionine-adenosyltransferase (MAT), to characterize the lipid and protein changes induced in peripheral nerve and brain myelin in rats during development. We also investigated the effect of exogenous SAMe by administering SAMe-1,4-butane disulfonate (SAMe-SD4). CL was given on days 7, 8, 12, and 13 and SAMe-SD4 was given daily from day 7; the animals were killed on day 18. CL accumulates in the brain reaching a concentration within 24 h compatible with its ID(50) in vitro and interacting with methionine metabolism; brain MAT activity and SAMe levels were lower and methionine levels higher than in controls. CL significantly reduced brain and nerve weight gains, brain myelin content, proteins, phospholipids, and galactolipids. Among phospholipids in nerve and brain, only sphingomyelin was significantly increased, by 35-50%. Sciatic nerve protein analyses showed some significant changes: protein zero in sciatic nerve remained unchanged but the 14.0- and 18.5-kDa isoforms of myelin basic protein showed a dramatic increase. Among the main proteins, in purified brain myelin, the proteolipid protein and dimer-20 isoform decreased after CL. SAMe-SD4 highlights some sensitive parameters by counteracting, at least partially, some alterations of PL--particularly galactolipids and sphingomyelins--and proteins induced by CL. The partial beneficial effects might also be explained by the age-related limited bioavailability of exogenous SAMe, a finding, to our knowledge, not yet reported elsewhere. This study demonstrates that availability of methyl donors is closely related to the formation of myelin components.

Effect of piribedil and its metabolite, S584, on brain lipid peroxidation in vitro and in vivo.

We studied the effect of piribedil (1-3,4-methylendioxybenzyl-4-(2-pyrimidyl) piperazine) and its catechol metabolite, S584 (1-(3,4-dihydroxybenzyl-4-(2-pyrimidinyl)-piperazine), on rat brain lipid peroxidation (a) in vitro in rat synaptosomes and cortical slices after induction of an oxidative stress and (b) in vivo in mouse brain after short-term exposure (two and three 4-h cycles) to O2/CO2 (95%:5%). The metabolite (10[-4]-10[-5] M), but not piribedil, prevented Fe3+-stimulated lipid peroxidation in rat synaptosomes and in rat cortical slices incubated with high oxygen concentrations. Piribedil (7.5 and 30 mg/kg, orally), counteracted the increase in thiobarbituric reactive substances in the brain of mice only when these were exposed to two or three cycles of a high oxygen concentration. S584 (30 mg/kg, orally) reduced thiobarbituric acid reactive substances in brain in mice exposed either to air (control) or to three cycles of a high oxygen concentration. These results suggest that piribedil has an antiperoxidative effect in brain, which may be partly related to the in vivo formation of the catechol metabolite, S584.

Reye syndrome model in rats: protection against liver abnormalities by L-carnitine and acetyl-L-carnitine.

The effects of L-carnitine (LCn) and acetyl-L-carnitine (AcLCn) were assessed on the liver alterations observed in Kilpatrick's model of Reye syndrome in rats; fasted rats were given lipopolysaccharide (LPS), 0.2 mg/kg i.p., 12 hr before they were sacrificed, plus acetylsalicylic acid (ASA), 50 mg/kg i.p., 11 hr before sacrifice; LCn or AcLCn were given twice, 500 mg/kg orally, 12 and 2 hr before sacrifice. LPS+ASA-treated rats showed a dramatic decrease of hepatic ketone bodies and acetyl-CoA and an increase of isobutyryl-CoA, isovaleryl-CoA and succinyl-CoA. Electron microscopy of LPS+ASA-treated rat liver showed a slight but significant alteration in mitochondrial inner structure. Because impairment of mitochondrial function in RS is associated with swelling, we investigated whether the microviscosity of mitochondrial lipids and the cholesterol-phospholipid ratio (CHOL/PL), were involved in the RS model used. Mitochondria from LPS+ASA-treated rats showed a decrease in lipid microviscosity, in CHOL/PL ratio and in CHOL/PL ratio of both inner and outer membrane fractions; these alterations suggested a general increase in membrane fluidity. LCn and AcLCn reversed the morphological alterations in mitochondria after LPS+ASA, observed by electron microscopy, the decrease in KB and the toxic increase in short-chain acyl-CoAs; AcLCn only reversed the decrease in acetyl-CoA. LCn and AcLCn prevented mitochondrial lipid alterations mainly in the inner membrane fraction.(ABSTRACT TRUNCATED AT 250 WORDS)